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YEAR 2 MED > Module 2A - Dermatology > Flashcards

Module 2A - Dermatology Flashcards

1
Q

Which cells predominantly make up the epidermis?

A

Keratinocytes –> migrate from lower epidermis (stratum basale)
- Once they reach the upper epidermis, they lose their nuclei and form tightly packed layers of keratin to form the stratum corneum

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2
Q

What is the top outer layer of the skin called –> what is it’s function

A

Epidermis –> barrier function

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3
Q

vicious cycle in eczema

A
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4
Q

Atopic eczema –> where does it usually affect + management

A
  • Flexor surfaces
    Management:
  • emollients –> regular use
  • topical steroids –> acute flares
  • phototherapy –> UVB
  • DMARDs
  • (if itchy –> antihistamines)
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5
Q

Emollients

A
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6
Q

Steroids and examples of use

A
  • lower potentency for delicate areas such as face or genitals –> hydrocortisone 1%
  • higher potency may be required for thicker skin areas like palm or soles –> betamethasone valerate 0.1%
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7
Q

Fingertip unit (FTU)

A
  • 1 fingertip unit (FTU) covers area size of 2 hands
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8
Q

scoring tools –> EASI and DLQI –> what condition they used in

A

atopic eczema

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9
Q

What type of hypersensitivity reaction is allergic contact dermatitis?

A

Type IV delayed hypersensitivity reaction
–> reactions tend to happen 48-72hrs after contact with the allergen

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10
Q
A

Contact dermatitis

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11
Q

Why would patch testing be used?

A

If unknown allergen/trigger of contact dermatitis

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12
Q

Contact dermatitis –> management

A
  • Avoid contact with allergen!
  • Liberal emollients
  • Topical steroids
  • Treat any secondary infection
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13
Q

Skin anatomy –> label

A
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14
Q

time frame

Acute vs chronic urticaria

A
  • Acute –> < 6 weeks
  • Chronic –> > 6 weeks
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15
Q

Urticaria pathophysiology:

____ ____ degranulation

  • type of hypersensitivity reaction
A

Mast cell

  • Type I hypersensitivity immediate reaction due to allergen –> IgE mediated
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16
Q

4 types of hypersensitivity reactions

A

Type I –> reaction mediated by IgE antibodies
Type II –> cytotoxic reaction mediated by IgG or IgM antibodies
Type III –> reaction mediated by immune complexes
Type IV –> delayed reaction mediated by cellular response (48-72hrs)

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17
Q

All atopic diseases are what type of hypersensitivity reaction?

A

Type I –> IgE mediated immune repsonses

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18
Q

what to avoid + medications

Urticaria management

A
  • Avoid trigger/allergen +/- treat infection + Avoid NSAIDs, aspirin, codeine
  • 2nd-gen H1 antihistamine (non-sedating) up to QDS –> cetirizine, loratadine
  • Sedating histamine at night –> eg. chlorphenamine
  • Next step is prednisolone 30mg –> 5-6 days
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19
Q

Test for type I hypersensitivity

A

Skin prick testing

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20
Q
  • Nodule
  • Papule
  • Pustule
  • Vesicle
  • Papule
A
  • Nodule = larger
  • Papule = smaller
  • Pustule = blob has pus in it
  • Vesicle = blob with fluid inside (clear)
  • Papule = blob of skin with nothing inside it
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21
Q

Herpes simplex pathogens

A
  • HSV-1 –> orofacial (80-90%)
  • HSV-2 –> genital (70-90%)
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22
Q

Herpes simplex management

A
  • Topical acyclovir 5% ointment
  • If systemic –> acyclovir 200mg x5 a day for 5 days
  • Prophylaxis –> acyclovir 200mg TDS for 6-12 months
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23
Q

Herpes zoster pathogen + aetiology

A
  • Varicella zoster virus (VZV)
  • reactivation of latent VZV in a sensory ganglia
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24
Q

Treatment for any herpes virus

Herpes zoster –> treatment

A
  • Acyclovir
  • can also give analgesia to relieve pain
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25
Q

treatment?

Viral warts pathogen

A

human papillomavirus (HPV)

–> benign condition no treatment

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26
Q

Molluscusm contagiosum pathogen

A

Molluscum contagiosum virus (MCV) –> poxvirus

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27
Q

Impetigo common pathogens

A

Staph. aureus and Strep. pyogenes

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28
Q

Impetigo –> treatment

A
  1. Clean –> hydrogen peroxide 1%
  2. Topical antibx –> fusidic acid
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29
Q

Folliculitis pathogens

A

Staph. aureus, Pseudomonas aeruginosa

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30
Q

2 bacteria that are infrequent resident flora of the skin

A

Staph. aureus and Strep. pyogenes

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31
Q

Cellulitis pathogens

A

Staph. aureus and Strep. pyogenes

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32
Q

Cellulitis –> treatment

A

beta-lactams –> penicillins and cephalosporins

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33
Q

Necrotising fascitis –> treatment

A
  • surgical debridement, or amputation
  • antibiotics –> gentamicin, clindamycin
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34
Q

Scabies pathogen

A

Sarcoptes scabiei var. hominis (human itch mite)

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35
Q

Scabies management

A

Skin lotions containing permethrin –> all family have to take

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36
Q

Tinea –> common organisms

A
  • Tinea verrucosum
  • Tinea rubrum
  • Micosporum canis
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37
Q

Tinea treatment

A

topical antifungals –> imidazoles

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38
Q

Tinea…
- corporis
- capitis
- pedis
- cruris

A
  • Tinea Corporis –> body
  • Tine Capitis –> head (note: can get ringworm scab thing on scalp)
  • Tinea Pedis –> feet
  • Tinea Cruris –> groin
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39
Q

Candida intertrigo pathogen

A

Yeast –> usually candida albicans

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40
Q

Candida… treatment

A

topical antifungals

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41
Q

Pityriasis Versicolor and Seborrhoeic dermatitis pathogen

A

Yeast –> Malassezia furfur

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42
Q

Pityriasis versicolor treatment

A
  • selenium sulphide shampoo (2.5%)
  • ketoconazole shampoo
  • or topical antifungals
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43
Q

A - HSV infection
B - Molluscum contagiosum
C - Folliculitis
D - Mucocutaneous leishmaniasis

A
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44
Q

A - HSV infection
B - Impetigo
C - Erysipelas/Cellulitis
D - Cutaneous leishmaniasis

A
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45
Q

IgE-mediated, Non-IgE-mediated, Non-allergic food hypersensitivity

Place into categories
- milk, egg, and peanut allergy
- Coeliac disease (gluten)
- Pollen related allergy
- lactose intolerance

A
  • IgE-mediated –> milk, egg, and peanut allergy + pollen related allergy
  • Non-IgE-mediated –> Coeliac disease (gluten)
  • Non-allergic food hypersensitivty (food intolerance) –> Lactos (milk) intolerance
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46
Q

Which T-helper cell is involved in IgE production, mast cell activation, and allergic disease?

A

Th-2

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47
Q

guttate psoriasis?

Psoriasis –> Management

A
  • Vitamin D3 analogues –> calcipotriol
  • Corticosteroids –> topical or oral
  • Coal tar –> soothes
  • Keratolytics (eg. salicylic acid) –> reduces scales –> enhances penetration of topical treatment
  • Phototherapy –> UVB, PUVA –> narrow-band UVB is best
  • Topical dithranol –> good for inflammation and over production of skin cells
  • Biologics –> anti-TNFs
    (Guttate psoriasis –> often spontaneously resolves within 2/3 months)
48
Q

UVA vs UVB

A
  • UVA –> causes ageing
  • UVB –> main carcinogen –> damages DNA and inhibits DNA repair processes
49
Q

Breslow thickness

A
  • Breslow thickness –> predicts melanoma survival (5 yr survival)
  • essentially how deep the cancer goes
50
Q

Glasgow 7-point checklist for melanoma

A
51
Q

Management of any suspected skin cancer

A
  • Skin excision biopsy –> histopathology
52
Q

Exclamation mark hair –> what condition

A

Alopecia areata

53
Q

Alopecia Totalis vs Alopecia Universalis

A
  • Alopecia Totalis –> total loss of scalp hair
  • Alopecia Universalis –> total loss of body hair
54
Q

Trichotillomania

A

Self-induced pulling of hair

55
Q

Hirsutism –> what is it + if symptoms of deep voice, increased muscle bulk, or clitoromegaly, then what are your next steps

A
  • Androgen-dependent hair growth in a female
  • urgently referred to endocrine for possible ovarian or adrenal tumour –> can also check for abdominal mass
56
Q

Nail problems:
- Clubbing –>
- Koilonychia –>
- Onycholysis –>
- Pitting –>

A
57
Q

Management of nail psoriasis

A
  • Potent topical steroid at base of nail/cuticle
  • Steroid injection into base of nail
58
Q

Hutchinson’s sign –> what condition?

A

Extension of pigmentation to nail fold –> acral lentiginous melanoma

59
Q
A
60
Q

size?

Papule vs pustule

A
  • Papules = measuring <5mm in diameter
  • Pustules = pus-filled spots
61
Q

size?

Nodulocystic acne –> more severe

A

Nodules = inflamed, swollen lesions >5mm

62
Q

2 skin changes seen in acne

A
63
Q

Grading of severity of acne

A
64
Q

Acne management

A
  • Benzoyl peroxide (gel or face wash) –> antiseptic –> reduces no. bacteria on skin
  • Topical retinoids (gel or cream) –> eg. tretinoin, adapalene –> works by keratinocyte proliferation –> removes dead skin cells from surface of skin (exfoliating) –> prevents building up within hair follicles
  • Topical antibiotics –> eg. erythromycin, doxy, clarithro
  • Combined oral contraceptive pill for females –> lowers androgen lvls –> less sebum and less severe acne
  • +/- Oral antibiotics (doxy, erytrho, clarithro)
  • Isotretinoin –> severe acne (specialist use)
65
Q

Acne –> when to refer to dermatology

A
66
Q

What pill that women sometimes take can make acne worse?

A

Progesterone only pills –> the lack of oestrogen may allow for higher lvls of androgen

67
Q

Diagnostic features of rosacea

A
68
Q

Rosacea management

A
  • 1st line –> topical ivermectin and oral doxycycline
69
Q

Pathogenesis of acne

A
  • Keratinocyte proliferation - leading to follicular plugs
  • Androgen-induced sebum production - usually occurs during puberty
70
Q

Most common side effect of topical steroids

A

Skin thinning

71
Q

Creams vs ointments

A
  • Ointments are oil-based
  • Creams are a mixture of oil and water
72
Q

How long should you wait between emollient application and topical steroids application

A

30 mins

73
Q
A
74
Q

Name 3 pre-cancerous lesions and treatment for each

A
  • Actinic keratoses, Bowen’s disease (SCC in situ), and lentigo maligna are all pre-cancerous lesions
  • Actinic keratoses + Bowen’s –> Efudix cream or 5-fluorouracil (topical chemo.) + cryotherapy
    (Curettage and cautery (C+C) can be used for Bowen’s)
  • Lentigo maligna –> imiquimod (immunosuppessive drug) or surgical excision
75
Q

Risk factors associated with skin cancer

A
76
Q
A
77
Q

+ treatment

Erythema nodosum causes

A
  • depends on cause –> eg. stopping causative drug, symptomatic treatment
  • if no cause –> bed rest + fluids
78
Q

Treatment of pyoderma gangrenosum

A

High-dose oral steroids

79
Q
A
  • Necrobiosis lipoidica –> associated with diabetes
80
Q
A
  • annular granuloma –> raised borders
  • associated with autoimmune and diabetes
  • usually self-limiting
81
Q

most common trigger

A
  • Erythema mulitforme - target lesions
  • most common triggers - infections (Herpes simplex)
82
Q

Treatment of a widespread erythematous rash

A

Moisturiser + topical steroid

83
Q
A
  • Fluid-filled blisters, erythematous patches
    –> Bullous pemphigoid
  • Skin biopsy
  • Management –> high dose oral prednisolone is mainstay, then can add potent topical steroids, azathioprine
84
Q
A
  • erythematous ulcerated patches from ruptured blisters
  • pemphigus vulgaris
  • skin biopsy
  • potent topical steroids, high dose oral prednisolone, azathioprine
85
Q
A
  • Dermatitis herpetiformis
  • Check TTG (tissue transglutaminase) –> coeliac blood test
  • Skin biopsy –> IgA deposition
  • Management –> gluten-free diet and topical steroids
  • Dapcin if coeliac diet doesn’t work
86
Q

Causes + investigations + management

A
87
Q

Wound healing video

A

Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=1VBLmyDjC0w

88
Q

Vitiligo is associated with…

A

Autoimmune diseases –> Addison’s, Type 1 diabetes

89
Q

Serious condition that eczema can develop into –> pt has red, rash, and outbreak of spots/inflammation + management

A
  • Eczema herpeticum
  • IV antivirals (aciclovir)
90
Q

Acne vulgaris drugs that are contraindicated in pregnancy

A

Tetracyclines and retinoids –> teratogenic

91
Q

Sebhorroeic dermatitis treatment

A
  • Corticosteroids
  • Scalp –> ketaconazole shampoo
  • Face/body –> topical antifungal (ketoconazole)
92
Q

Pityriasis rosea often follows a…

A

Viral infection

93
Q

Drugs known to exacerbate psoriasis

A
  • Lithium
  • Anti-malarials
  • Beta-blockers
  • ACEi
  • anti-TNF-alpha
  • NSAIDs
94
Q

TEN (toxic epidermal necrolysis) –> 4 classes of drugs that can cause crossreactions leading to TENs

A
  • Beta-lactam antibiotics –> penicillin, cephalosporin and carbapenem (penicillins –> co-amoxiclav)
  • Sulph- drugs
  • Anticonvulsants –> carbamazepine, phenytoin
  • NSAIDs
95
Q

SJS vs TEN

A
  • SJS –> < 10% of body affected by rash
  • TEN –> > 30% of body affected by rash

(overlap in between)

96
Q

A 62-year-old female is referred to dermatology by her GP due to a lesion over her shin. It initially started as a small red papule which later became a deep, red, necrotic ulcer with a violaceous border. What is the likely diagnosis?

A

Pyoderma gangrenosum

97
Q

Shingles (herpes zoster) –> treatment + timeline to start treatment within

A

Oral antivirals –> within 72hrs onset

98
Q

Vitamin D (Calcitriol) –> functions + how is it acquired

A
  • Important for bones –> increases dietary calcium and phosphate absorption
  • Acquired from UV skin exposure (up to 15 mins per day) and Diet
  • Vitamin D deficiency common –> it is important to give people advice about sun protection but also advise vit D supplements
99
Q

Why are transplant patients at an increased risk of skin cancer?

A
  • due to immunosuppression
100
Q

What are the two main types of albinism?

A

Oculocutaneous albinism:
- Type 1: more severe - no melanin
- Type 2: some melanin

  • Ocular albinism: normal, or slightly paler than normal eyes for their ethnicity, skin, and hair
101
Q

Actinic keratoses –> pathology + aetiology + location on body

A
  • Proliferation of cytologically aberrant epidermal keratinocytes
  • UV-induced + very common in bald white men over 75yrs
  • Sun-exposed areas –> scalp
102
Q

BCC –> pathogenesis + mutations in what gene predispose to BCC

A
  • Basal Cell Carcinoma (aka. rodent ulcer) is the most common cancer in humans, derived from non-keratinising cells originating in the basal layer of the epidermis
  • mutations in the PTCH gene
103
Q

Erythema migrans –> what disease + management

A
  • Lyme disease
  • Antibiotics (doxy, amox)
104
Q

Impetigo –> most common causative pathogen + management

A
  • Staph. A or Strep. pyogenes
    1. Clean –> hydrogen peroxide 1% cream
    2. Topical antibiotics –> fusidic acid
105
Q

Gorlin’s syndrome predisposes to what skin cancer?

A

BCC

106
Q

Alopecia ariata management

A
  • 80-90% will spontaneously regrow
  • consider –> topical corticosteroids, topical minoxidil
107
Q

Dermatitis herpetiformis –> underlying pathophysiological process + skin biopsy finding

A

Formation of IgA antibodies –> skin biopsy shows a granular pattern of IgA deposition

108
Q

Impetigo vs Measles –> isolation periods

A
  • Impetigo –> isolate until 48hrs after starting treatment (fusidic acid) and should have crusted over
  • Measles –> isolate for 4 days after rash appears
109
Q

Most common side effect of oral isotretinoin

A

Dry skin

110
Q

What drug type is known to exacerbate plaque psoriasis?

A

Beta-blockers

111
Q

What gene is associated with eczema?

A

Filaggrin gene

112
Q

Biopsy and immunofluorescence showing IgG auto-antibody deposits within the epidermis
VS
Biopsy and immunofluorescence would show IgG auto-antibodies deposited on the basement membrane

  • Pemphigus vulgaris vs bullous pemphigoid
A
  • Pemphigus –> deposits within epidermis
  • Bullous pemphigoid –> deposits on basement membrane
113
Q

Nikolsky sign positive suggests

A

Pemphigus Vulgaris

114
Q

Psoriasis –> which drug may be used long term

A

Calcipotriol (vit D3 analogue)
–> reduces epidermal proliferation, reduces scale and thickness of plaques, but doesn’t help with erythema

115
Q
A

YEAR 2 MED (16 decks)

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