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Year 3 GP > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Describe the six skin types

A

I - Always Burns, Never Tans
II - Always Burns, Sometimes Tans
III - Sometimes Burns, Always Tans
IV - Never Burns, Always Tans
V- Dark Brown, rarely burns, fast and easy tanning
VI- Black, Almost never burns

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2
Q

Using the mnemonic SCAM - how would you describe an individual lesion?

A

Size (and shape)
Colour
Associated secondary change
Morphology (and margin)

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3
Q

Using the mnemonic ABCD - how would you describe a pigmented lesion?

A

Asymmetry
(Irregular) Border
Colour (two or more)
Diameter (>6mm)

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4
Q

Define: Lesion, Rash, Naevus, Comedone

A

Lesion - area of altered skin
Rash - an eruption
Naevus - Localised malformation of tissue, commonly pigmented
Comedone - blocked hair follicle/pore containing altered sebum/bacteria and cellular debris. Can be open (blackheads) or closed (whitehads)

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5
Q

What is the Koebner Phenomenon in dermatological distribution?

A

Linear eruption

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6
Q

Define the following Dermatological Configuration terms: Discrete, Confluent, Target, Annular, Discoid

A

Discrete - Separate Lesions
Confluent - Lesions merging together
Target - Concentric rings like a dartboard
Annular - Circle/Ring (like ringworm)
Discoid - Coin shaped

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7
Q

Describe Erythema

A

Redness due to inflammation and vasodilation, that blanches under pressure

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8
Q

Describe Purpura

A

Red/Purple discolouration due to bleeding into skin/mucous membrane that does not blanch with pressure
Can be Petichae (small pinpoint) or Ecchymoses (large bruise)

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9
Q

What is the difference between Hypopigmentation and Depigmentation?

A

Hypopigmentation - areas of paler skin (eg Pityriasis Versicolor)
Depigmentation - White skin due to lack of melanin (eg Vitiligo)

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10
Q

Define the morphological terms: Macule, Patch and Plaque

A

Macule - flat area of altered colour (freckles)
Patch - larger flat area of altered colour
Plaque - Palpable scaling raised lesion>0.5cm in diameter

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11
Q

Define the morphological terms: Papule and Nodule

A

Papule - Solid raised lesion <0.5cm (eg Xanthomata)
Nodule - Solid raised lesion >0.5cm

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12
Q

Define the morphological terms: Vesicle and Bullae

A

Vesicle - Raised clear fluid filled lesion <0.5cm
Bullae - Raised clear fluid filled lesion>0.5cm

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13
Q

Define the morphological terms: Pustule and Abscess

A

Pustule - Pus containing lesion<0.5cm in diameter
Abscess - Localised accumulation of pus in dermis or subcut tissue

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14
Q

Define the morphological terms: Wheal, Furuncle, Carbuncle

A

Wheal - Transient raised lesion due to dermal oedema
Furuncle - Staph infection in or around a hair follicle
Carbuncle - Staph infection around adjacent follicle

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15
Q

Define: Excoriation, Lichenification and Scaling

A

Excoriation - loss of epidermis following trauma
Lichenification - well defined roughening of skin with accentuation of skin markings
Scaling - Flakes of Stratum Corneum

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16
Q

Describe three different scar complications

A

Atrophic - thinning
Hypertrophic - Hyperproliferation within wound boundaries
Keloidal - Hyperproliferation beyond wound boundary

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17
Q

Define Ulcer and Fissure

A

Ulcer - Loss of dermis and epidermis
Fissure - Epidermal crack due to excess dryness

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18
Q

What is Hypertrichosis?

A

Non androgen dependent pattern of hair growth

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19
Q

Define: Koilonychia, Oncholysis, Pitting

A

Koilonychia - Spoon depression of nail plate
Oncholysis - Separation of distail nail from nail bed (psoriasis, fungal nail function)
Pitting - Depression in nail plate (psoriasis, eczema)

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20
Q

Describe the four different special cells of the skin

A

Keratinocytes (protective barrier)
Langerhans (immunological)
Melanocytes (protects cell nuclei from UV)
Merkel Cells (specialised nerve endings for sensation)

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21
Q

Describe the four main layers of the epidermis

A

Stratum Corneum - Keratin
Stratum Granulosum
Stratum Spinosum - Prickle Cell
Stratum Basale - Actively dividing cells

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22
Q

What is the ‘extra’ layer of the epidermis and where is it found?

A

Stratum Lucidum - Paler compact keratin
In areas of ‘thick skin’ (eg soles of feet)

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23
Q

Describe the composition of the Dermis

A

Made collagen/elastin/GAGs
Contains immune cells, nerves, lymphatics and blood supply

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24
Q

What are the three main types of hair?

A

Lanugo - Fine long hair in foetus
Vellus - Fine short hair on body’s surface
Terminal - Coarse long hair on scalp/eyebrows/eyelashes

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25
Q

What are Sebaceous Glands?

A

Produce sebum via hair follicles
Lubricates and waterproofs skin
Stimulated by androgens

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26
Q

What are Sweat Glands? State the two types.

A

Innervated by sympathetic nervous system
Eccrine - Universally distributed in skin
Apocrine - located in axilla and genitalia etc and function from puberty onswards

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27
Q

Describe the pathophysiology of Urticaria

A

Mast cell releases mediators causing locally increased permeability of capillaries and venules
Involves only epidermis

can be acute or chronic
can be inducible (aquagenic, solar, cold induced)

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28
Q

How would you manage Urticaria?

A

Trigger avoidance - consider skin prick testing, skin biopsy, bloods and antibody testing

Try and avoid medication where possible
Antihistamines (6 weeks non-sedating such as loratidine)
Corticosteroids if severe

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29
Q

What is Angio-Oedema? How would you manage it?

A

Swelling of epidermis AND dermis

Stable and mild - no management
Stable and moderate - 6 weeks antihistamines
Progressing - IM hydrocortisone and chlorphenamine

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30
Q

Describe Hereditary Angio-Oedema and give two other causes of non allergic angio-oedema

A

Autosomal dominant deficiency of C1 esterase inhibitor (which normally aims to prevent reactviation of compliment system)
Causes recurrent swelling
Treated by C1 Esterase Inhibitor Concentrate (found in FFP)

Idiopathic (more likely if autoimmune), non-allergic drug reaction - eg to ACE

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31
Q

What is Anaphylaxis?

A

Bronchospasm, facial and laryngeal oedema

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32
Q

How would you manage Anaphylaxis?

A

1) A to E approach , lie down , elevate legs, remove triggers
2) Adrenaline (if in community - 500mcg 1:1000 IM, monitor response, if inadequate repeat, then continue to repeat every 5 minutes until resolution)
3) Consider nebulised salbutamol/mgso4 for wheeze
4) After resolution consider Hydrocortisone or chlorphenamine

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33
Q

What is Erythema Nodosum? Give 4 causes

A

Hypersensitivty reaction to a variety of stimuli causing inflammation of fat cells under skin
Strep Pyogenes, TB, Malignancy, IBD

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34
Q

How does Erythema Nodosum present?

A

Tender nodules usually on shins , after 2 weeks leave bruise like discolouration as they resolve
50% may experience arthralgia or morning stiffness

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35
Q

How do you manage Erythema Nodosum

A

Generally self limiting
Cool compresses and bed rest
NSAIDs
Treat underlying cause

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36
Q

Over 50% of Erythema Multiforme is caused by HSVI and HSVII, give a non infective cause

A

Drugs - Barbiturates, Penicillins, Sulfonamides, NSAIDs

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37
Q

Describe the presentation of Erythema Multiforme

A

Rash begins on extremities, symmetrically
Initially a dull red macule that develops a central papule/bullae to form a target lesion

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38
Q

How would you manage Erythema Multiforme?

A

Self Limiting
Analgesics and Steroid Creams

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39
Q

What is Steven Johnson’s Syndrome?

A

A severe form of Erythema Multiforme, caused by hypersensitivity reaction normally to drugs such as Allopurinol/Carbemazepine/Penicillins

At least two mucosal sites involved

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40
Q

How might Steven Johnson Syndrome present?

A

May have a prodromal phase
Mucocutaneous Lesions (Erythema Multiforme)
May have other organ involvement (Dysuria, Conjunctivitis, Mouth Ulcers)

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41
Q

Describe four different managements for Steven Johnson Syndrome

A

Remove offending cause
Supportive
Immunomodulation (potentially pulsed steroids to avoid poor wound healing)
Plasmphoresis

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42
Q

What is SCORTEN?

A

Predicts mortality for Steven Johnson Syndrome
Score greater than 3 requires ITU

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43
Q

What is Erythroderma? Give four causes.

A

Exfoliative dermatitis involving atleast 95% skin’s surface

Previous skin disease, Lymphoma, Drugs (Penicillin, Allopurinol), Idiopathic

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44
Q

How might Erythroderma present?

A

Skin appears inflamed, oedematous and scaly
Pt feels systemically unwell with malaise and lymphadenopathy

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45
Q

How would you manage Erythroderma? Give 3 complications.

A

Emollients and wet wraps to maintain skin’s moisture
Topical steroids

Hypothermia, Secondafry Infection, High Output Heart Failure

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46
Q

What is Eczema Herpeticum?

A

Rare and serious skin infection caused by Herpes Simlex Virus
Many possible complications so treated as an emergency

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47
Q

How does Eczema Herpeticum present? How would you manage it?

A

Systemically unwell with extensive crusted papules/blisters/erosions
Antivirals (Acyclovir)

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48
Q

What is Necrotising Fasciitis?

A

Rapidly progressing infection of the deep fascia causing necrosis of subcutaneous tissue

Normally caused by Group A Strep, or a mixture of aerobic and anaerobic

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49
Q

How does Necrotising Fasciitis present?

A

Severe pain, Erythema, Tachycardia, Crepitus (Subcutaneous Emphysema)

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50
Q

How would you manage Necrotising Fasciitis?

A

Extensive Surgical Debridement
IV Antibiotics

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51
Q

Define Cellulitis

A

Spreading bacterial infection of the skin involving the deep subcutaneous tissue and dermis

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52
Q

What is the difference between Cellulitis and Erysipelas?

A

Erysipelas is a more superficial form
Erysipelas has more sharply demarcated borders than Cellulitis

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53
Q

Give 5 risk factors for Cellulitis/Erysipelas

A

IVDU
Elderly
Venous Insuffiency
Lymphoedema
Alcoholism

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54
Q

Erysipelas is mainly caused by Strep Pyrogenes, name the causative organisms of Cellulitis.

A

Staph Aureus
Post Op - Strep Pyogenes, Closdtrodium Perfringes (crepitus)

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55
Q

How would you manage Cellulitis/Erysipelas?

A

Rest, Elevation and Analgesia
Uncomplicated - Flucloxacillin 500mg QTS
Facial Involvement - Co _ Amoxiclav

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56
Q

What is Staphylococcal Scalded Syndrome?

A

Scald appearance seen in infancy and early childhood
Caused by epidermolytic strain of toxigenic STaph Aureus

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57
Q

How might Staphylococcal Scalded Syndrome present?

A

Scald appearance followed by large bullae
Painful lesions
Lesions on buttocks/hands/feet/face (perioral crusting)

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58
Q

How would you manage Staphylococcal Scalded Syndrome?

A

Flucloxacillin (or Vancomycin for MRSA)
Analgesia
Petroleum Jelly

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59
Q

Describe Tinea Corporis and Tinea Cruris

A

Corporis - Fungal infection of Trunk/Limbs, ittchy circular lesions with raised edges
Cruris - same as corporis but in groin and natal cleft

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60
Q

Describe Tinea Manuum and Tinea Pedis

A

Tinea Manuum - Fungal infection of hands
Tinea Pedis - Athlete’s Foot
Scaling and fissuring dryness

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61
Q

Describe Tinea Capitus and Tinea Unguium

A

Capitis - Scalp Ringworm (patches of broken hair, scaling and infammation)
Unguium - Fungal infection of the nail causing yellowed discoloration/thickened/crumbly nail

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62
Q

What is Tinea Incognito?

A

Due to inappropriate treatment of fungal infection with steroid creams
Ill defined and less scaly

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63
Q

What is Ptyriasis/ Tinea Versicolor?

A

Cutaneous infection with the yeast Malassezia Furfur
Causes scaly brown patches on upper trunk that fail to tan on sun exposure

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64
Q

State the two non melanoma skin cancers

A

Basal Cell Carcinoma
Squamous Cell Carcinoma

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65
Q

Give 3 risk factors of skin cancer

A

Age
UV exposure
Type I skin

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66
Q

Describe the presentation of nodular BCC (TURP)

A

T- Telangiectasia
U- Ulceration
R- Rolled Edges
P- Pearly

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67
Q

What is Squamous Cell Carcinoma?

A

Locally invasive malignant tumour of keratinocytes with the ability to metastasise

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68
Q

Name 3 pre malignant conditions that are a risk factor for SCC?

A

Actinic Keratoses (ie sun spots)
Bowens Disease
Leukoplakia

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69
Q

How do Squamous Cell Carcinomas present?

A

Keratotic
Ill defined
Potentially ulcerating

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70
Q

Describe four managements of Skin Cancer

A

Surgical Excision
Radiotherapy
Cryotherapy/Cautery
Mohs Micrographic Surgery

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71
Q

What is Mohs Micrographic Surgery

A

Borders progressively excised until free of tumour microscopically
Good for cosmetically sensitive areas

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72
Q

What is a Malignant Melanoma?

A

Invasive malignant tumour of epidermal melanocytes with the ability to metastasise

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73
Q

Describe the four types of Malignant Melanoma

A

Superficial Spreading - common on lower limbs
Nodular Melanoma - Common on trunk
Lentigo Maligna Melanoma - common on face in elderly due to long term cumulative exposure
Acral Lentigous Melanoma - Palms, soles and nail beds

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74
Q

What is the Breslow Thickness?

A

The risk of recurrence of Malignant Melanoma
The thicker the melanoma the higher the risk

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75
Q

Describe the presentation of Atopic Eczema

A

Usually develops in childhood and resolves during adulthood
Itchy erythematous dry scaly patches normally on flexor aspects (but can be on face and extensor aspects in infants

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76
Q

Give 5 other dermatological features of atopic eczema

A

Excoriation
Lichenification
Nail pitting
Hypo/Hyperpigmentation
Chronic lesions - dry and scaly (erythematous or grey/brown)

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77
Q

Name two conservative managements of Eczema

A

Avoid triggers (such as wool/synthetic fibres and extremes of temperature)
Frequent emollients

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78
Q

Give 3 pharmacological managements for Eczema

A

Topical Therapies - topical steroids (for flares) or topical immunomodulators (tacrolimus)
Oral therapies - antihistamines
Immunosupressants for severe non responsive cases

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79
Q

State three secondary viral infectons of Eczema

A

Molluscum Contagiosum
Viral Warts
Eczema Herpeticum

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80
Q

What is Acne Vulgaris?

A

Inflammatory disease of pilosebaceous follicles
Due to androgens there is increased sebum production which subsequently causes them to become blocked

81
Q

What is Propionibacterium Acne?

A

Bacterial colonisation and inflammation of sebaceous glands

82
Q

Acne Vulgaris can be non inflammatory or inflammatory . Describe the appearance of both

A

Non Inflammatory - Open and closed comedones
Inflammatory - Papules/postules/nodules/cysts

83
Q

Describe three topical therapies for Acne Vulgaris

A

Benzoyl Peroxide - reduces sebum production and growth of P.Acnes (may cause burning sensation)
Topical Abx - Clindamycin/Tetracycline (normally combined with another therapy)
Topical Retinoids - Tretinoin, anti inflammatory (contraindicated in pregnancy)

84
Q

How long do systemic treatments for Acne take to work?

A

3-4 months

85
Q

Describe three oral treatments for Acne

A

Lymecycline/Doxycycline (erythro if preg)
Anti-Androgens - COCP
Oral Isotretinoin (VERY TOXIC)

86
Q

What is Psoriasis?

A

Chronic Inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration

87
Q

Describe the pathophysiology of Psoriasis

A

Injury/infection increases pro-inflammatory markers such as IL6 and TNF
APC activated which then activate TH1 and TH17
Abnormal keratinocyte differentiation (decreasing keratinocyte transit time)

88
Q

State four subtypes of Psoriasis

A

Chronic Plaque (most common)
Guttate (raindrop lesions, post strep)
Seborrhoeic (scalp and behind ears, blepharitis)
Pustular (plantar, palmar)

89
Q

How does Psoriasis present? Describe two extra-epidermal manifestations.

A

Well demarcated erythematous scaly plaques, common on extensor surfaces and scalp
Nail changes (pitting,oncholysis) and Psoriatic Arthropathy

90
Q

What is Auspitz Sign?

A

Scratch and gentle scale removal causes capillary bleeding in Psoriasis

91
Q

Describe two oral and two topical therapies for Psoriasis

A

Topical - Vitamin D Analogues (Calcipitriol), Topical Steroids
Oral - Methotrexate, Retnoids

92
Q

Name a complication of Psoriasis

A

Erythroderma

93
Q

What determines blister fragility?

A

Depends on the level of split within the skin
More fragile - intraepidermal
Less fragile - subepidermal

94
Q

What is Bullous Pemphigoid?

A

Immunobullous blistering (subepidermal) condition usually affecting the elderly

95
Q

How will Bullous Pemphigoid present?

A

Tense fluid filled blisters on an erythematous base, often itchy
Normally affects trunk or limbs

96
Q

How do you manage Bullous Pemphigoid?

A

Topical steroids for local disease
Oral therapies for widespread (steroids, tetracycline)

97
Q

What is Pemphigus Vulgaris?

A

Immunobullous blistering (intraepidermal) condition usually affecting the middle aged

98
Q

How will Pemphigus Vulgaris present?

A

Flaccid and easily ruptured blisters, often painful and affecting mucosal areas

99
Q

How would you manage Pemphigus Vulgaris?

A

High dose steroids
Immunosupressants

100
Q

Scabies is an itchy rash caused by a parasitic mite, give four risk factors.

A

Overcrowding
Poverty
Homelessness
Poor Hygiene

101
Q

How does Scabies present?

A

Signs and symptoms don’t develop for 3-4 weeks
Widespread itching (worse at night and when warm)
Papular/Vesicular lesions at burrow sites

102
Q

How do you investigate Scabies?

A

Usually just clinical
Ink Burrow Test - Ink rubbed over burrow and wiped with an alcohol wipe, ink should track the burrow sites

103
Q

Describe four management points for Scabies

A

All close contacts should be treated on the same day to avoid reinfestation
Topical Parasiticidal Cream (Permethrin) applied head to toe once a week
Wash clothes/towels/bedding
Antihistamines for itching

104
Q

How does Senile Purpura present?

A

Elderly population with sun damaged skin
Extensor surfaces of hands and forearms

105
Q

Describe the presentation of a Venous Ulcer (including common sites)

A

Large shallow and irregular usually in malleolar area
Exudative and granulating base
Pain on standing

106
Q

How would you manage a Venous Ulcer?

A

Compression bandaging

107
Q

Describe the presentation of an Arterial Ulcer (including common sites)

A

Small and sharply defined with a deep necrotic base
Abent peripheral pulses, shiny skin and loss of hair
Pain at night/elevation of leg

108
Q

How would you manage an Arterial Ulcer?

A

Vascular Reconstruction

109
Q

What is ABPI? What do values indicate?

A

Ankle Brachial Pressure Index, compares peripheral blood flow
Normal is 1-1.4
If less than 0.8 it is suggestive of arterial insufficiency

110
Q

Describe the presentation of a Neuropathic Ulcer (including common sites)

A

Often painless, variable in size and shape
Granulating base
Often in pressure sites (heels, soles, toes)
Can be Neuroischaemic

111
Q

How would you manage a Neuropathic Ulcer?

A

Wound debridement
Regular repositioning
Good nutrition
Appropriate footwear

112
Q

What is a Dermatofibroma?

A

Benign mass, often mistaken for a more serious pathology, following on from insect bites such as mosquitos

113
Q

State the two layers of the dermis

A

Papillary
Reticular

114
Q

Describe the relevance of a skin lesion (suspected malignancy) itching and bleeding respectively

A

Itching - Perineural Invasion
Bleeding - Ulcerative component

115
Q

When would you do a punch lesion of a suspicious lesion?

A

If it was in a cosmetically sensitive area

116
Q

Name 5 subtypes of BCC

A

Nodular
Superficial (can appear like dermatitis)
Morphoeic
Pigmented
Basosquamous

117
Q

Apart from pre-malignant conditions, give three risk factors specific for SCC

A

Viral Infections
Chronic Wounds
Psoriasis Treatment

118
Q

What is Bowen’s Disease?

A

In- Situ SCC disease (pre-malignant condition)
Erythematous plaques and sharp borders

119
Q

Name four types of SCC

A

Ulcerative
Verrucous
Marjdins (arising from chronic wounds)
Subungal (underneath nail bed)

120
Q

What is Gorlin Syndrome?

A

Autosomal Dominant condition increasing risk of BCCs. Presents as Multiple BCCs

121
Q

What is Rosacea?

A

Chronic relapsing disease of facial skin characterised by flushing episodes, persistent erythema, telangiectasia, papules and pustules

122
Q

What is a common presentation of Rosacea in men?

A

Rhinophyma - enlarged nose

123
Q

What is the first line management for Rosacea?

A

Topical Metronidazole

124
Q

How does Lichen Planus present?

A

Affects flexor surfaces of wrists/forearms/legs
Intensely itchy 2-5mm red/violet shiny topped pamphlet (Wickham Striae)
Mucous Membranes - White raises trabecular lesions

125
Q

How is Lichen Planus managed?

A

Topical Steroids if required

126
Q

What is Toxic Epidermal Necrolysis?

A

Similar to Steven Johnson Syndrome

Normally drug induced

Full thickness epidermal necrosis with superior dermal detachment

127
Q

Name 6 management options for BCC

A

Surgical excision (with 4mm border)
Moh’s micrographic surgery
Radiotherapy
Cryotherapy/Cautery
Photodynamic therapy
Topical Imiquimod

128
Q

Give three risk factors for Malignant Melanoma

A

UV exposure
Type 1 Skin
Dysplastic Naevus Syndrome

129
Q

Name three prognostic factors for Malignant Melanoma

A

Breslow Thickness
Ulceration
Mitoses

130
Q

Describe the step up management for Eczema

A

Mild - Liberal emollient and Hydrocortisone cream

Moderate - Liberal emollient and Betamethasone/Clobetasone (consider antihistamines)

Severe - Same as moderate plus oral steroids

131
Q

How does Acne present in darker skin?

A

Hyperpigmented

Less Erythematous

132
Q

When can you refer patients to Dermatology for consideration of commencing Isotretinoin in Acne?

A

If the patient has tried two different antibiotics for three months each

133
Q

Name three long term effects of Acne

A

Scarring
Pigmentation issues
Psychological effects

134
Q

Describe the NICE step up management for Chronic Plaque Psoriasis

A

Emollients

1) Potent Steroid and Calcipitriol for four weeks
2) If no improvement after 8 weeks then Calcipitriol BD
3) If no improvement after 8-12 weeks then potent steroid BD for up to 4 weeks or coal tar preparation

135
Q

What are the secondary care management options for Chronic Plaque Psoriasis?

A

Phototherapy (three times a week, can cause skin ageing/SCC)

Systemic therapies such as Methotrexate or Cyclosporin

136
Q

How is Psoriasis of the Scalp managed?

A

Potent topical steroids once daily for four weeks

If unresponsive try a different formula, or try physically removing scales first

137
Q

How is Face/Flexural/Genital Psoriasis managed?

A

Mild to Moderate potency steroid for maximum two weeks

138
Q

What is Vitiligo?

A

Acquired depigmenting disorder where there is complete loss of melanocytes (thought to be autoimmune)

139
Q

How does Vitiligo present?

A

At any age

Single or multiple patches of depigmentation (often symmetrical)

Exhibits Koebner phenomenon

140
Q

Describe the management options for Vitiligo

A

Minimise skin injury (could trigger a new patch)

Topical Steroids and Tacrolimus

UVB Phototherapy

Oral Immunosupressants

141
Q

What is Melasma?

A

Acquired chronic skin disorder where there is increased skin pigmentation

Caused by genetic predisposition + trigger (eg COCP, Pregnancy, Sun exposure)

142
Q

How does Melasma present?

A

Brown macules with irregular borders

Symmetrical

Normally forehead, upper lip and cheeks

143
Q

How is Melasma managed?

A

Lifelong sun protection
Cosmetic camouflage
Topical Hydroquinone/Vitamin C

144
Q

What is Lichen Planus?

A

Pruritic Papular Eruption most likely T cell mediated in origin

Associated with Trauma/Hep B/Hep C/PBC

145
Q

How does Lichen Planus present?

A

Acute, affecting flexor surfaces

Intensely itchy 2-5mm red shiny topped papule with white streaks (Wickham’s Striae)

May get blisters

146
Q

How does Lichen Planus present on hands and feet?

A

Firm and yellow papules

147
Q

How does Lichen Planus present on mucous membranes?

A

White slightly raised lesions with trabecular appearance (can be asymptomatic or painful)

148
Q

How is Lichen Planus managed?

A

May not require - may self resolve in 1y

Moderately potent steroids and sedating antihistamines

Topical steroids for oral lichen planus

If resistant - immunosupression

149
Q

What is the main complication of Lichen Planus?

A

Oral SCC

150
Q

What is Seborrhoeic Dermatitis?

A

Common benign scaling skin rash, commonly affecting areas rich in sebaceous glands (face/scalp/chest)

151
Q

Describe the pathophysiology of Seborrhoeic Dermatitis

A

Inflammatory reaction to Malassezia Yeast

More common in Parkinson’s and HIV

Associated Pityriasis Captis (Dandruff)

152
Q

How does Seborrhoeic Dermatitis present on the scalp?

A

Associated fine scaling

Dry pink patches with bran like scale

153
Q

How does Seborrhoeic Dermatitis present on the face?

A

Inflamed, greasy with fine scaling

Commonly affecting nasolabial folds, bridge of nose, blepharitis

154
Q

How does Seborrhoeic Dermatitis present on the chest?

A

Papules and greasy scales

155
Q

How is Seborrhoeic Dermatitis of the scalp managed?

A

Remove thick crusts or scales with Olive Oil

Ketaconazole shampoo atleast twice a week for a month

156
Q

How is Seborrhoeic Dermatitis of the face/chest managed?

A

Ketoconazole cream daily for 2-4 weeks

Intermittent Hydrocortisone/Tacrolimus

157
Q

What is Rosacea?

A

Chronic relapsing disease of facial skin, characterised by facial flushing with persistent erythema/telangiectasia/papules/pustules

158
Q

Describe the pathophysiology of Rosacea

A

Chronic acneiform disorder of pilosebaceous glands with increased capillary reactivity to heat

159
Q

How does Rosacea present?

A

Intermittent flushing progressing to constant (triggered by changes in temp/alcohol/caffiene/spice)

Skin isn’t greasy/may be dry

160
Q

Describe the non medical management of Rosacea

A

Reassurance
Avoiding precipitating factors
Daily sun screen
Cosmetic camouflage

161
Q

Describe the medical management of Rosacea

A

Avoid topical steroids

Flushing - Brimonidine (topical alpha agonists)

Mild - Ivermectin
Mod/Severe - Add Doxycycline

Telangiectasia - laser therapy
Rhinophyma - requires surgery

162
Q

What is Rhinophyma?

A

Large nose occurring almost exclusively in men secondary to Rosacea

163
Q

Tuberous Sclerosis is the systemic formation of Hamartomas. Describe four dermatological manifestations

A

Ash Leaf Macules (areas of depigmentation on the trunk)

Facial Angiofibroma (small red nodule)

Shagreen Patches (orange peel patches over sacrum and back)

Skin tags

164
Q

Neurofibromatosis is an Autosomal Dominant disorder. Name four dermatological manifestations

A

Cafe au Lait spots
Axillary/Inguinal Freckles
Hypopigmented macules
Benign Cherry angiomas

165
Q

Name three skin disorders of Pregnancy

A

Atopic Eruption of Pregnancy

Polymorphic Eruption of Pregnancy

Pemphigoid Gestationis

166
Q

What is Atopic Eruption of Preganancy?

A

Very common

Eczematous itchy white rash

Doesn’t require any specific treatment

167
Q

What is Polymorphic Eruption of Pregnancy?

A

Pruritic condition associated with last trimester

Lesions often appearing in abdominal striae

Can give emollients/topical steroids/oral steroids depending on severity

Piriton for the itch

168
Q

What is Pemphigoid Gestationis?

A

Pruritic blistering lesions often starting in periumbilical region and spreading

Rarely seen in first pregnancy or first trimester

Normally requires oral steroids

169
Q

Actinic Keratoses are thickened scaly growths caused by sunlight. Describe the pathophysiology

A

Characteristic UV mutations

Atypical pleomorphic keratinocytes in basal layer

Confined to epidermis

Can progress to Bowens or SCC

170
Q

How does Actinic Keratoses present?

A

Sun exposed areas

Small rough spots that can enlarge to become red and scaly

171
Q

How is Actinic Keratoses diagnosed?

A

With a Dermatoscope

Grade 1 - slightly palpable
Grade 2 - moderately thick
Grade 3 - very thick, hyperkeratotic
Field Damage - multiple AKs on a background of erythema and sun damage

172
Q

Emollients and Sun Protection should be used in Actinic Keratoses. What other management options are there?

A

Topical 5FU
Diclofenac Gel
Imiquimod
Ablative

173
Q

Bowen’s Disease is SCC in situ. Give four risk factors

A

Sun damage
Radiation
Arsenic
HPV

174
Q

How does Bowen’s disease present?

A

-Slow growing, erythematous hyperkeratotic patch/plaque with an irregular border
-Size related to duration
-Asymptomatic but may bleed

175
Q

How can Bowen’s disease be managed?

A

Topical 5FU
Cryotherapy
Photodynamic therapy
Surgical excision

3% untreated will progress to invasive SCC

176
Q

What is a Keratocanthoma?

A

Rapidly growing squamoproliferative lesions that look like well differentiated SCCs

Grow rapidly over few weeks to months, and then spontaneously resolve over 4-6m

177
Q

How to Keratocanthomas present?

A

Solitary round firm skin coloured/red papules progressing to domes

May have central ulceration or Keratin plug

178
Q

How are Keratocanthomas investigated?

A

Excisional biopsy under 2ww as can’t distinguish from SCC

179
Q

How can Keloid Scars be managed?

A

Intralesional Steroids
Pressure/Occlusive dressings
Surgical removal is a risk as it may be bigger than before

180
Q

What is the purpose of Emollients? Name a possible SE

A

Rehydrates skin and re-establishes surface lipid layer
Can be used as a soap substitute

May have irritant/allergic reaction

181
Q

Describe steroids in terms of potency

A

Mild - Hydrocortisone
Moderate - Clobetasone (Eumovate)
Potent - Betamethasone (Betnovate)
Very Potent - Clobetasol Proprionate (Dermovate)

182
Q

Name three local and three systemic side effects of steroids

A

Local - Skin Atrophy, Telangiectasia, Striae

Systemic - Cushings, Hypertension, Immunosupression

183
Q

Name three side effects of Aciclovir

A

GI upset
Raised LFTs
Reversible neruological reactions

184
Q

Name one sedating and one non sedating antihistamine

A

Non Sedative - Loratidine
Sedative - Chlorpheniramine

185
Q

Name a topical antiseptic

A

Chlorhexidine

186
Q

Name four SE of Oral Retinoids

A

Dry Skin/Lips/Eyes

Disordered LFTs

Hypercholesterolaemia

Depression

187
Q

Describe two local and two systemic effects of Biologic therapies

A

Local - Redness, Swelling

Systemic - Allergy, Flu like

188
Q

Describe the step up management for Eczema

A

Mild - Emollients and Hydrocortisone

Moderate - Emollients, Betamethasone/Clobetasone, consider antihistamines or topical tacrolimus

Severe - moderate plus consideration of oral steroids or phototherapy

189
Q

How would you manage Tinea Capitus

A

If signs of a Kerion - refer to Dermatology

Oral Terbinafine and Ketoconazole Shampoo

189
Q

How would you manage Tinea Corporis?

A

If mild, Topical Terbinafine/Clotrimazole (if inflammatory can add in Hydrocortisone)

If moderate to severe use Oral Terbinafine

190
Q

How would you manage Tinea Pedis medically?

A

Mild - Topical Terbinafine +/- Steroids

Mod to Severe - Oral Terbinafine

191
Q

What general management advice should you give someone with Tinea Pedis?

A

-Keep feet dry
-Well fitting footwear and clean cotton socks
-Dispose of any shoes that may contain fungal spores
- Wear socks/footwear in public areas such as pools

192
Q

How is Tinea Unguium managed?

A

Only if Symptomatic (difficulty walking)/Cosmetically distressed/Immunocompromised

If 1 or 2 nails affected - Topical Amorolfine for up to a year

More than 2 nails affected then Oral Terbinafine (Dermatophytes) or Itraconzaole (Yeasts)

193
Q

What general management advice should you give patients with Tinea Unguium?

A

Keep nails short
Don’t share nail clippers with other members of the family
Dispose of any shoes which may contain fungal spores

194
Q

How are topical steroids measured?

A

Finger Tip Units

1 finger tip unit = 0.5 grams = covers twice that of a flat adult hand

195
Q

How is Isotretinoin monitored?

A

Serum LFTs and Lipids before starting, after one month of treatment, and then every three months thereafter

196
Q

Why can you not combine Isotretinoin and Doxycycline?

A

Will cause Idiopathic Intracranial Hypertension

197
Q

What is the Eron Classification?

A

For cellulitis

I - not systemically unwell and no comorbidities
II - systemically unwell OR systemically well with comorbidities
III - Severely systemically unwell or profound comorbidities
IV - sepsis or necrotising fasciitis

198
Q

What is the relationship between melanoma and vitamin D?

A

High levels of circulating vitamin D are associated with reduced progression of melanoma, therefore these levels should be optimal when commencing treatment

Year 3 GP (6 decks)

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