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conditions Flashcards

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Dermatology Board Prep flashcards
1
Q

What is Dermatitis Herpetiformis

A

chronic immunobullous condition associated with coeliac disease

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1
Q

Dermatitis Herpetiform epidemiology

A
  • Young adults (15-40year olds)
  • Caucasians
  • More common in males
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2
Q

Dermatitis Herpetiform

Aetiology

A
  • Autoimmune disease in pxs with gluten intolerance
  • Risk factors: coeliac disease, family hx of autoimmune
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3
Q

Dermatitis Herpetiform

Pathophysiology

A
  • Intolerance to gliadine part of gluten causes autoimmune reaction in patient
  • IgA molecules are released into circulation before migrating to skin and creating the appearance of this disease
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4
Q

Dermatitis Herpetiform

Histophysiology

A
  • Papillary dermal micro abscesses
  • Subepidermal blisters
  • Neutrophil + eosinophil infiltrates in the dermal papillae
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5
Q

Where is gluten found

A
  • barley
  • rye
  • wheat
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6
Q

Dermatitis Herpetifrom

presentation

A

Small clusters of vesicles +/or papules:
- Present on knee + elbow extensor surfaces, scalp + buttocks
- Symmetrical distribution
- Extreme pruritus

GI Symptoms of coeliac disease
- Fatigue
- Steatorrhea
- Diarrhoea
- Bloating
- Weight loss
- Pale stools

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7
Q

Dermatitis Herpetiform

Diagnosis

A
  • Skin biopsy (direct immunofluorescence shows granular IgA deposits in dermal papillae)
  • tTG IgA antibody testing
  • Duodenal biopsy (if coeliac disease suspected)
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8
Q

Dermatitis Herpetiform Managment

A
  • GF diet
  • Topical steroids (symptomatic relief)
  • Dapsone (for rash + pruritis)
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9
Q

Type of cancer associated with dermatitis herpetiform

A

Small bowel lymphoma

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10
Q

PEMPHIGUS VULGARIS

Definition

A

Autoimmune condition characterised by intraepithelial blistering of skin + mucous membranes

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11
Q

PEMPHIGUS VULGARIS

epidemiology

A
  • 50-60yr olds
  • Ahkenazi Jews + Indians
  • Ppl affected by other autoimmune conditions
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12
Q

PEMPHIGUS VULGARIS

Aetiology

A
  • Idiopathic aetiology, occurs spontaneously
  • Genetic influence
  • Speicifc triggers (Drugs, malignancy, infection, Trauma)
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13
Q

PEMPHIGUS VULGARIS

Pathophysiology

A
  • Circulating IgG molecules attack (the protein desmoglein 3) found within desmosomes holding keratinocytes together at the bottom of the epidermis
  • Separating keratinocytes from eachother
  • Fluid-filled blister appears
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14
Q

PEMPHIGUS VULGARIS

Histopathology

A
  • Intra-epidermal blistering (basal layer stays stuck to dermis)
  • Supra basal clefts + blisters containing acantholytic cells
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15
Q

PEMPHIGUS VULGARIS

Diagnosis

A
  1. Positive Nikolsky Sign
  2. Skin biopsy
    - Acantholytic cells present
    - Immunofluorescnes shows intracellular deposits of IgG on surface of keratinocytes throughout epidermis (chicken wire pattern)
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16
Q

PEMPHIGUS VULGARIS

Management

A
  1. Local (topical steroids + topical anaesthetics)
  2. Systemic (prednisolone)
  3. May need other specialties invovled (eg. opthamology)
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17
Q

PEMPHIGUS VULGARIS

prognosis

A
  • relapsing + remitting course
  • Stop treatment during inactive disease periods + restart during flare ups
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18
Q

BULLUS PEMPHIGOID

Definition

A

A rare, subepidermal blistering disease of autoimmune aetiology.

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19
Q

BULLUS PEMPHIGOID

EPIDEMEOLOGY

A
  • Elderly (rare <50)
  • Common in elderly w neurological conditions (like parkinsons, stroke and dementia)
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20
Q

BULLUS PEMPHIGOID

aetiology

A
  • HLA associations (Suggesting genetic element)
  • Idiopathic + spontaneous cause
  • Possible triggers (medication, Injury, Skin infection)
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21
Q

BULLUS PEMPHIGOID

Pathophysiology

A
  • IgG (IgE + Tcells also involved) attacks BP180 + BP230 proteins in BM of epidermis causing an acute inflam response (incl. neutrophil recruitment, complement activaation + release of proteolytic enzymes)
  • This causes destruction of hemidesmosomes + later formation of subepidermal blisters
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22
Q

BULLUS PEMPHIGOID

histopathology

A
  • Eosinophils prominent
  • Subepidermal cleft w. obvious inflam infiltrates (eg. neutrophils + T cells)
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23
Q

BULLUS PEMPHIGOID

presentation

A
  1. Pruritus and erythema - (may precede blistering onset by months)
  2. Large, tense bullae.
    - few or many
    - located anywhere (often flexures)
    - may burst and become crusted erosions
  3. Sparing of mucosal surfaces.
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24
Q

BULLUS PEMPHIGOID
diagnosis

A
  1. Negative Nikolsky sign
  2. Skin biopsy => Subepidermal blistering (full thickness epidermis as blister roof)
  3. Antibody testing
    - Indirect IMF for circulating BP180/BP230 antibodies
    - Direct IMF shows antibodies along basement membrane
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25
Q

BULLUS PEMPHIGOID

Management

A
  1. Oral Prednisolone (MAIN TREATMENT)
  2. Antibiotic therapy (Tetracyclines)
  3. Topical steroids (potent or v potent)
  4. Antihistamines (for pruritus)
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26
Q

BULLUS PEMPHIGOID

Why are tetracycline antibiotics used

A

They have anti-inflam effect + are steroid sparing agents

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27
Q

What is negative Nikolsky sign

A

Rub skin, top layer will not shear off

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28
Q

Hair types

A
  • Lanugo
  • Vellus
  • Terminal
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29
Q

What is scarring alopecia

A

follicles lost

30
Q

What is non-scarring alopecia

A

Hair follicles still present (Can regrow)

31
Q

Examples of non-scarring localised hair loss

A
  • Alopecia areata
  • Androgenetic (pattern alopecia)
  • Trichotillomania
  • Traction Alopecia (due to hair stlying)
  • Tinea capitis (Scalp fungal infection)
32
Q

Examples of localised scarring alopecia

A
  • Burns/Trauma
    -Chronic discoid lupus (CDLE)
  • Lichen Planus
  • Frontal fibrosing alopecia
33
Q

Causes of generalised hair loss

A
  • Telogen effluvium (eg. sever illness, stress, childbirth)
  • Endocrine (eg. thyroid disease)
  • Drugs
  • Dietary deficiency (eg. iron, zinc, vit D)
  • Diffuse alopecia areata
  • Malnutrition
  • Androgenetic alopecia
33
Q

Is generalised hair loss normally scarring or non-scarring

A

Non-scarring

34
Q

Investigations for hair loss

A
  1. for fungal exam:
    - Skin scraping
    - Hair plucking
    - Woods lamp examination (some fungal species flourescent)
  2. general look at hair folicles
    - Dermoscopy
    - Scalp biopsy +/- Immunofluorescence
    - Blood tests (FBC, TFTs, Iron/Zinc levels, Hormone profile)
35
Q

What is this

A

alopecia areata

  • circular areas of hair loss
  • preservation of hair follicles
  • Broken hair, tapering hair
36
Q

Process of alopecia areata

A
  • Autoimmune
  • normal recovers itself (takes months to years to recover)
  • recurrent episodes/extensive involvement = less likely to regrow
37
Q

What is it called when alopecia areata affects:

  • whole scalp
  • Whole body
A
  1. Alopecia totalis
  2. Alopecia universalis
38
Q

Pharmacological treatment for alopecia areata

A
  • Topical steroids
  • IL steroids
  • Wig provision
39
Q

what is this?

A

Trichotillomania

  • self-induced hair loss (hair pulling)
  • Asymmetrical
  • Associated with psychological issues
40
Q

What is this

A

Tinea capitis

fungal infection of scalp

41
Q

Tinea Capitis investigations

A

skin scraping
hair plucking
woods lamp

42
Q

Tinea capitis treatment

A

oral anti-fungal agent

43
Q

Tinea capitis epidemeology

A

pre-pubertal kids
areas of poverty/overcrowded living

44
Q

What is kerion

A

Dramatic tinea capitis - big immune response to fungal infection

45
Q

Kerion identifiers

A
  • Abscess formation
  • More inflamed
  • Localised scarring hair loss
46
Q

What is this

A

Chronic Discoid Lupus Erythematosus

47
Q

DCLE Diagnosis

A

clinical + biopsy with DIF

48
Q

DCLE treatment

A
  1. Potent topical steroids
  2. hydroxychloroquine
    always - photoprotection
49
Q

Androgenetic/Pattern hair loss stages in men + women

A
  • Localised problem

Males: Generally starts at resection at temples then vertex of scalp then it joins together)

Women: front of hair margin preserved, general thinning across scalp)

50
Q

Androgenetic hair loss investigation

A

hormone levels
iron
zinc

51
Q

Androgenetic hair loss treatment

A
  • Minoxidil (regaine) (vasodilator, stops when not in use)
  • Anti-androgens (common for females with PCOS)
  • If extensive, wig
52
Q

Hair excess broad categories

A
  • Hirsutism
  • Hypertrichosis
53
Q

Hirsuitism
- Definition

A
  • Excess hair growth in females in male distribution due to ^ androgen levels or ^ end organ response to normal androgen levels
54
Q

Causes of hirsutism

A
  1. Familial/constitutional - associated w seborrhoea, acne, androgenetic alopecia
  2. Hormonal - eg.PCOS/Androgen secreting tumour
55
Q

Hirsutism investigation

A
  1. History + exam
    - Ask about other signs of androgen excess (eg. irregular menstrual cycle, acne, difficulty conceiving)
  2. Hormone profile
  3. Ovarian US if indicated
56
Q

What is hypertrichosis

A

Excessive hair growth in a non-adrogenic distribution

56
Q

Hypertrichosis causes

  1. Local
  2. General
A
  1. Naevi (moles), occult spina bifida (indicated by faun tail sign), Chronic scarring/inflammation
  2. Malnutrition, Anorexia, Prophyria, occult malignancy, drugs (eg. minoxidil, phenytoin, cyclosporin)
57
Q

What causes Beau’s line

A

caused by transient arrest in nail growth which occurs during acute stress/illness

58
Q

What condition may they have

A

Psoriasis

  • Nail pitting
  • Dystrophy
  • Subungual hyperkeratosis
  • Onikolysis
  • Oil drop sign
59
Q

Normal nail label

A
60
Q

What causes acute paronychia

A

Staph aureus
Strep pyogenes

61
Q

What is this

A

Acute paronychia

62
Q

Acute paronychia treatment

A
  • drain it
  • oral Antibiotics
63
Q

What causes chronic paronychia

where is it commonly seen

A
  • Candida / can be mould-related
  • people who commonly deal with water
64
Q

Chronic paronychia

A

topical or oral antifungals
protect skin from being wet all the time

65
Q

What is this

A

fungal nail infection

  • onicholysis
  • subungual hyperkeratosis
66
Q

Investigations for fungal nail infection

A

Nail clipping

67
Q

Treatment for fungal nail infection

A
  • Topical anti-fungal nail varnish
  • Oral antifungal agent used for 3-6months if extensive disease (eg.Terbinafine)
68
Q

What is this

A

Subungual haematoma

  • normally due to trauma
69
Q

Subungual haematoma treatment

A
  • Let it grow out over time
  • hole can be bore in nail to relieve pressure which is source of pain
70
Q

what is this

A

malignant melanoma

NB - Hutchinson’s sign (spreading pigmentation)

71
Q

What is this

A

myxoid cyst

  • at proximal nail fold
  • accumulation of synovial fluid
  • gutter effect in nail due to (pressures growing nail)

Derm (8 decks)

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