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Year 4 Medicine > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Define toxic epidermal necrolysis

A

Potentially life-threatening dermatological disorder characterised by widespread erythema, necrosis and bullous detachement of epidermis and mucous membranes

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2
Q

What is the milder form of TEN called?

A

Stevens-Johnson syndrome (<10% involvement)

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3
Q

What are the risk factors for TEN?

A

Children
HIV/AIDS
Drugs

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4
Q

What drugs can cause TEN?

A 
Sulphonamides
Phenobarbital 
Carbamazepine
Lamotrigine
Allopurinol
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5
Q

What is the aetiology of TEN?

A

Adverse drug reaction
Infection
Vaccination
Graft vs host disease

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6
Q

What are the symptoms of TEN?

A

Prodrome of cough, myalgia and anorexia 2-3 days before
Itching
Burning
Fever

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7
Q

What are the examination findings in TEN?

A

Involvement of mucosa and internal epithelial surfaces

Nikolsky’s sign

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8
Q

What is Nikolsky’s sign?

A

Slight rubbing of the skin results in exfoliation - occurs in TEN

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9
Q

What investigations can be done for a patient with suspected TEN?

A

Bloods - FBC, U&Es, CRP
Skin biopsy
Blood cultures

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10
Q

How is TEN managed?

A

ITU, burn, gynae, ophthalmology involvement
Stop all drugs
Analgesia and fluids
IVIG

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11
Q

What are the differential diagnoses for TEN?

A

Bullous pemphigoid

Bullous pemphigus

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12
Q

What are the complications of TEN?

A 
Death 
Dehydration/malnutrition
ARDS
GI ulceration/perforation
Infection 
Sepsis
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13
Q

What is the prognosis of TEN?

A

30-50% mortality

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14
Q

Define erythema multiforme

A

Acute hypersensitivity rash caused by infection or drugs

Usually mild but makor form can affect mucous membranes

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15
Q

What are the risk factors for EM?

A

History of EM or infection
Suspect drugs
Vaccinations - diphtheria, tetanus

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16
Q

What is the aetiology of EM?

A 
HSV
EBV
Drugs - sulphonamide, anticonvulsants
Mycoplasma
Autoimmune 
HIV
Wegener's
Carcinoma, lymphoma
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17
Q

What features are seen on examination of a patient with EM?

A

Erythematous polycyclic/annular/concentric rings (target lesions)
May blister
Symmetrical rash

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18
Q

What investigations can be done for a patient with suspected EM?

A

Bloods - FBC, U&Es
Serology - HSV, VZV
M.pneumoniae titre
CXR

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19
Q

How is EM managed?

A

Treat underlying cause
Recurrent - aciclovir
Resistant - azathioprine

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20
Q

What are the differential diagnoses of EM?

A

TEN

SJS

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21
Q

What are the complications of EM?

A

Sepsis
Cellulitis
Permanent skin/eye damage and scarring
Inflammation of internal organs

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22
Q

What is the prognosis of EM?

A

Usually self-limiting

Can recur

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23
Q

How can EM be prevented?

A

Prophylactic antivirals for HSV

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24
Q

Define acute urticaria

A

Development of itchy weals/swellings in the skin due to leaky dermal vessels
AKA hives

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25
Q

What is the difference between urticaria and angio-oedema?

A

Angio-oedema involves sub-dermal vessels; life-threatening

Urticaria involves dermal vessels

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26
Q

What are the types of urticaria?

A 
Cold
Pressure 
Stress
Heat/cholinergic
Solar 
Aquagenic 
Contact
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27
Q

What are the risk factors for urticaria?

A

Atopy

Young age

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28
Q

What is the aetiology of urticaria?

A 
Autoimmune 
Viral/parasitic infection
Drug reaction
Food allergy
SLE
Idiopathic
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29
Q

What drugs can cause urticaria?

A

NSAIDs
Penicillin
ACEi
Opiates

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30
Q

What would be the examination findings of a patient with urticaria?

A

Cutaneous swellings/weals, develop over a few minutes anywhere on the body and resolve spontaneously in minutes/hours
Lesions are intensely itchy and erythematous

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31
Q

How is urticaria managed?

A 
Treat underlying cause 
Avoid salicylates and opiates 
Oral antihistamines (e.g. cetirizine)
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32
Q

How is angio-oedema managed?

A

IM adrenaline

IV steroids

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33
Q

What are the differential diagnoses for urticaria?

A

Blisters
Dermatitis
Insect bite
Drug reaction

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34
Q

What are the complications of urticaria?

A

Anaphylaxis

Airway blockage

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35
Q

What is the prognosis of urticaria?

A

Usually spontaneously resolves

May become chronic

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36
Q

How can urticaria be prevented?

A

Prophylactic antihistamines for predisposed individuals

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37
Q

Define erythroderma

A

Clinical state of inflammation/redness of all/most of the skin

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38
Q

What are the risk factors for erythroderma?

A

Male

Older age

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39
Q

What is the aetiology of erythroderma?

A 
Atopic eczema Psoriasis 
Drugs 
Seborrhoeic eczema 
Idiopathic 
Rare - leukaemia, HIV, toxic shock syndrome
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40
Q

What drugs can cause erythroderma?

A 
Sulphonamides
Gold
Sulfonylureas
Penicillin
Allopurinol
Captopril
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41
Q

What are the symptoms of erythroderma?

A

Tight, itchy skin
Malaise
Pyrexia
Widespread lymphadenopathy

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42
Q

What signs are seen on examination of a patient with erythroderma?

A

Hair loss
Ectropion
Nail shedding
Pustules

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43
Q

How is erythroderma investigated?

A

Skin biopsy

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44
Q

How is erythroderma managed?

A 
Keep patient warm 
Regular observation and fluid balance 
Swab for infection 
Stop drugs
Bed rest
Emollient/mild topical steroid
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45
Q

What are the complications of erythroderma?

A 
Death 
Cardiac failure 
Hypothermia 
Fluid loss
Hypoalbuminaemia 
Capillary leak syndrome
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46
Q

Define impetigo

A

Highly contagious superficial bacterial infection with yellow crusting most common in children

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47
Q

What are the risk factors for impetigo?

A

Age 2-5
Crowded conditions (schools)
Warm, humid weather
Broken skin

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48
Q

What bacteria are most commonly implicated in impetigo?

A

S.aureus

Group A β-haemolytic streptococcus

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49
Q

What does impetigo look like on examination?

A

Weeping, exudative areas with honey-coloured crust

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50
Q

How is impetigo investigated?

A

Nasal swabs (resistant infection)

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51
Q

How is impetigo managed?

A

Topical fusidic acid or oral antibiotics

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52
Q

What are the differential diagnoses for impetigo?

A

Bullous impetigo

Scabies

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53
Q

Give a complication of impetigo

A

Cellulitis

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54
Q

What is the prognosis of impetigo?

A

Self-limiting and mild

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55
Q

How can impetigo be prevented?

A

Good personal hygiene

Avoid direct contact with affected

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56
Q

Define tinea

A

Superficial fungal infection of skin/nails by dermatophytes

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57
Q

What is tinea more commonly known as?

A

Ringworm

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58
Q

Give a risk factor for tinea

A

Immunosuppression

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59
Q

What are the 3 main organisms implicated in tinea?

A

Microsporum
Epidermophyton
Trichophyton

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60
Q

What does tinea look like on examination?

A

Asymmetrical, scaly patches with central clearing
Advancing, scaly, raised edges
Vesicles/pustules may be present

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61
Q

How can tinea be investigated?

A

Skin scrapings

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62
Q

How is tinea managed?

A

Topical terbinafine or systemic terbinafine/itraconazole

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63
Q

What are the differential diagnoses for tinea?

A

Nummular eczema
Granumola annulare
Psoriasis
Contact dermatitis

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64
Q

What are the complications of tinea?

A

Bacterial superinfection

General invasion of dermatophyte infection

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65
Q

What is the prognosis of tinea?

A

Curable

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66
Q

How can tinea be prevented?

A

Good skincare

Not sharing things with people who are affected

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67
Q

Define soft tissue abscess

A

Infection in the dermis/fat with development of walled off infection

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68
Q

What 2 organisms are most commonly implicated in soft tissue abscesses?

A

S.aureus

S.pyogenes

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69
Q

How are soft tissue abscessed managed?

A

Surgical drainage

Antibiotics if severe infection

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70
Q

Define cellulitis

A

Infection involving the dermis, mostly on the lower limb

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71
Q

What 2 organisms are most commonly implicated in cellulitis?

A

S.aureus

β-haemolytic streptococci

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72
Q

How do patients with cellulitis present?

A

Fever, unwell

Hot, tender area

73
Q

How is cellulitis managed?

A

IV flucloxacillin for 3-5 days followed by oral therapy for 2 weeks

74
Q

What are the differential diagnoses for cellulitis?

A

Animal bites
DVT
Dermatitis

75
Q

What organism is responsible for causing streptococcal toxic shock?

A

Group A β-haemolytic streptococci (primary infection of throat/skin)

76
Q

How does streptococcal toxic shock present?

A

Localised infection, fever and shock

Diffuse, faint rash over whole body

77
Q

How is streptococcal toxic shock managed?

A

Surgery - drain abscess
Antibiotics - penicillin, clindamycin
IVIG (severe)

78
Q

Define necrotising fasciitis

A

Immediately life-threatening, rapidly progressive soft tissue infection with deep tissue involvemtn

79
Q

How does necrotising fasciitis present?

A

Rapidly progressive
Pain out of proportion to clinical signs
Severe systemic upset
Visible necrotic tissue

80
Q

What late signs can be seen on imaging of necrotising fasciitis?

A

Fascial oedema

Gas in soft tissues

81
Q

How is necrotising fasciitis treated?

A

Surgical debridement

Broad spectrum antibiotics

82
Q

What are the 2 types of necrotising fasciitis?

A

Type 1 - polymicrobial, existing wound

Type 2 - group A streptococci, healthy tissue

83
Q

What are the 2 types of herpes simplex virus?

A

Type 1 - cold sores

Type 2 - genital herpes

84
Q

How is HSV diagnosed?

A

Clinically
Blood/vesicle fluid PCR
Serology

85
Q

How is HSV managed?

A

Aciclovir

86
Q

How is varicella zoster virus infection managed?

A

Supportive

At risk adults (pregnant, immunocompromised, pneumonitis) should be treated with 48 hours of symptoms with aciclovir

87
Q

Define eczema

A

Group of skin disorders causing dry, irritated skin

88
Q

List the different types of eczema

A 
Atopic 
Seborrhoeic 
Varicose 
Pompholyx
Contact 
Photoreaction
89
Q

What is the pathophysiology of eczema?

A

Abnormalities in skin barrier lead to increased permeability

90
Q

What are the risk factors for eczema?

A

Family history
Hygiene hypothesis
Exacerbating factors
Atopy

91
Q

What is the aetiology of eczema?

A

Genetic - loss of function mutation of FLG gene (codes for filaggrin protein)

92
Q

What signs are seen on examination of eczema?

A

Itchy, erythematous, scaly patches
Commonly in flexures
Acute lesions may weep/exude and have vesicles
Scratching causes excoriations and repeated rubbing causes lichenification

93
Q

What are the associated features of eczema?

A

Keratosis pilaris
Hyperlinear palms
Ichthyosis vulgaris

94
Q

How is eczema investigated?

A

Clinical diagnosis
IgE RAST
Allergy testing/skin prick
Swabs and scrabes

95
Q

How is eczema managed?

A

General - avoid triggers, good skincare
Topical - emollients, soap substitutes and steroids
Oral - antibiotics, antihistamines
Immune - tacrolimus

96
Q

How are steroids classified by potency in dermatology?

A

Mild > moderate > potent > super potent

97
Q

How are emollients classified by viscosity in dermatology?

A

Ointments vs creams vs lotions

98
Q

What second-line agents can be used to manage eczema?

A

UV phototherapy
Immunosuppressants - azathioprine, ciclosporin, methotrexate
Oral retinoids - alitretinoin

99
Q

What are the differentials for eczema?

A

Psoriasis
Scabies
Tinea

100
Q

What are the complications of eczema?

A

Secondary skin infection - S.aureus, viral warts
Conjunctival irritation, cataracts
Retarded growth in children

101
Q

What is the prognosis of eczema?

A

Spontaneous clearance in most children

Late onset more chronic with remitting/relapsing pattern

102
Q

How can eczema be prevented?

A

Secondary - moisturise, avoid sudden temperature change, reduce stress, avoid harsh fabrics/soaps

103
Q

What are the 4 main types of leg ulcer?

A

Venous
Arterial
Neuropathic
Pressure

104
Q

What is the pathophysiology of venous leg ulcers?

A

Sustained venous HTN in superficial veins causes incompetent valves in deep/perforating veins causing fibrin deposition and poor oxygenation of surrounding skin

105
Q

What is the pathophysiology of arterial leg ulcers?

A

Reduced arterial blood flow causes decreased tissue perfusion and poor healing

106
Q

What is the pathophysiology of neuropathic leg ulcers?

A

Repeated trauma over a pressure point

107
Q

What is the pathophysiology of pressure leg ulcers?

A

Skin ischaemia from sustained pressure over a bony prominence

108
Q

What are the risk factors for venous leg ulcers?

A 
Older age
FH
Venous disease 
Orthostatic occupation 
Smoking 
DVT
Female 
Increasing parity
109
Q

What are the risk factors for arterial leg ulcers?

A

Smoking
Diabetes
HTN

110
Q

What are the risk factors for neuropathic leg ulcers?

A

Peripheral neuropathy - diabetes
Foot deformity
Concurrent vascular disease

111
Q

What are the risk factors for pressure leg ulcers?

A

Prolonged immobility
Decreased sensation
Vascular disease
Poor nutrition - anaemia, hypoalbuminaemia, vitamin C/zinc deficiency

112
Q

What drug can cause leg ulcers?

A

Hydroxycarbamide

113
Q

What infections can cause leg ulcers?

A

TB
Deep mycoses
Syphilis
Yaws

114
Q

What features of the history indicate an arterial ulcer?

A

Pain

CV features - claudication, HTN, angina, smoker

115
Q

What features of the history indicate a pressure ulcer?

A

Old/immobile/unconscious
Pain of continued pressure
Hospital acquired

116
Q

What is seen on examination of a venous leg ulcer?

A

Gaiter area between medial malleolus and mid-calf
Oedma
Haemosiderin deposition - hyperpigmentation
Lipodermatosclerosis
Atrophie blanche - shiny white scarring
Telangiectasia

117
Q

What is seen on examination of a arterial leg ulcer?

A

Lateral aspect of leg or on foot
Punched out appearance
Leg cold and pale, hair loss, absent peripheral pulses
Surrounding skin shiny white

118
Q

What is seen on examination of a neuropathic leg ulcer?

A

Pressure areas (e.g. metatarsal heads)
Surrounded by callus
Deep
Insensate

119
Q

What is seen on examination of a pressure leg ulcer?

A

Painful and warm
Exudative, foul odour
Non-blanching discolouration

120
Q

How is a suspected venous ulcer investigated?

A

Duplex US - check for reflux

121
Q

How is a suspected arterial ulcer investigated?

A

Vascular assessment
Doppler USS
ABPI

122
Q

How is a suspected neuropathic ulcer investigated?

A

Bloods - glucose, HbA1c
US
ABPI
X-ray foot

123
Q

How is a suspected pressure ulcer investigated?

A

Clinical diagnosis

Wound swab, WCC, biopsy

124
Q

How is a venous ulcer managed?

A

High compression bandaging and leg elevation

Analgesia

125
Q

How is an arterial ulcer managed?

A

Keep clean and covered
Analgesia
Vascular reconstruction

126
Q

How is a neuropathic ulcer managed?

A

Remove pressure

Good footcare

127
Q

How is a pressure ulcer managed?

A

Keep pressure off bony areas
Adequate nutrition
Analgesia

128
Q

What are the differentials for leg ulcers?

A

Different types of leg ulcers
Squamous cell carcinoma
Pyoderma gangrenosum
Lymphoedema

129
Q

What are the complications of venous leg ulcers?

A

DVT
Haemorrhage
Infection

130
Q

What are the complications of arterial leg ulcers?

A

Infection
Tissue necrosis
Amputation

131
Q

What is the prognosis of venous leg ulcers?

A

80% healed in 6 months

132
Q

How can venous leg ulcers be prevented?

A

Avoiding prolonged sitting/standing
Exercise
Smoking cessation

133
Q

How can pressure ulcers be prevented?

A

Tissue viability nurses identify and assess those at risk

134
Q

Define psoriasis

A

Common skin disorder characterised by well-dermarcated scaly red plaques due to increased skin turnover

135
Q

What is the Koebner phenomenon?

A

Development of psoriasis at sites of skin trauma

136
Q

What is the pathophysiology of psoriasis?

A

T cell mediated autoimmune response causing inflammation and hyperproliferation of the skin

137
Q

What are the risk factors for psoriasis?

A 
Age (16-22 and 55-60)
FH
Drugs
Stress
Smoking 
Alcohol
Causasian
138
Q

What drugs can contribute to psoriasis?

A

Lithium
Antimalarials
Beta-blockers

139
Q

What is the aetiology of psoriasis?

A

Genetics - PSORS 1 gene

Environment

140
Q

What features of a history would indicate psoriasis?

A 
Fluctuating course 
Itching, bleeding 
Pain 
Family history 
Known triggers
141
Q

What features would be found on examination of psoriasis?

A

Pink/red well circumscribed plaques with silver scale
Extensor surfaces affected, plus back/ears/scalp
Associated - nail dystrophy, psoriatic arthritis, metabolic syndrome

142
Q

What nail features are associated with psoriasis?

A

Pitting
Onycholysis
Discolouration
Subungual hyperkeratosis

143
Q

How is psoriasis investigated?

A

Clinial diagnosis

Skin biopsy

144
Q

How is psoriasis managed?

A 
Education 
Emollients 
Topical therapy - steroids, vitamin D analogues, tacrolimus, coal tar, retinoid, dithranol 
UV therapy - B or A with psoralen 
Systemic - methotrexate, actirectin
Biologics - adalimumab
145
Q

What are the differentials for psoriasis?

A 
SLE
Pityriasis rosacea 
Seborrhoeic dermatitis
Eczema 
Lichen planus
146
Q

What are the complications of psoriasis?

A 
CV disease 
Psoriatic arthritis 
Depression/anxiety 
Lymphoma 
Secondary infection
147
Q

What is the prognosis of psoriasis?

A

Chronic, life-long

Relapses and remits

148
Q

How can psoriasis be prevented?

A

Secondary control of flare-ups - moisturise, reduce stress, avoid triggers

149
Q

Give 4 types of psosiasis

A

Chronic plaque
Flexural
Guttate
Erythrodermic/pustular

150
Q

What are the main features of flexural psoriasis?

A

Later in life
No scaling
Large flexures - groin, natal cleft, sub-mammary
Often misdiagnosed as candida

151
Q

What are the main features of guttate psoriasis?

A

Raindrop lesions
Children and young adults
Explosive eruptions over trunk
Triggered by strep throat

152
Q

What are the main features of pustular psoriasis?

A

Severe, life-threatening
Malaise, pyrexia, circulatory disturbance
Pustules are sterile collections of inflammatory cells

153
Q

Define acne vulgaris

A

Formation of comedones, papules, pustules, nodules, and/or cysts as a result of obstruction and inflammation of pilosebaceous units

154
Q

What is the pathophysiology of acne vulgaris?

A

Increased androgens -> increased sebum -> P.acnes overgrowth -> pustule
Genetic susceptibility -> blockage of duct -> comedones -> papule -> pustule

155
Q

What are the risk factors for acne vulgaris?

A 
Adolescence (12-24)
Genetic predisposition 
Greasy skin type 
Precipitating drugs
PCOS
Female
156
Q

What drugs can precipitate acne vulgaris?

A 
Androgens 
Steroids 
Antiepileptics 
Lithium
ACTH
157
Q

What is the aetiology of acne vulgaris?

A

Multi-factorial

Proprionibacterium acnes

158
Q

What features are found on examination of acne vulgaris?

A

Face and upper torso
Non-inflammatory open comedones (blackheads) and closed comedones (whiteheads)
Inflammatory papules, pustules, nodules, cysts
Scars - raised/hypertrophic or depressed/pitted

159
Q

How is acne vulgaris investigated?

A

Clinical diagnosis

Hormone levels, bacterial culture

160
Q

How is mild acne vulgaris managed?

A 
Comedones = topical retinoid or salicylic acid
Inflammatory = topical retinoid + topical antimicrobial
161
Q

How is moderate acne vulgaris managed?

A

Oral antibiotic + topical retinoid +/- benzoyl peroxide/OCP

162
Q

How is severe acne vulgaris managed?

A

Oral isotretinoin
OR
High-dose oral antibiotic + topical retinoid + benzoyl peroxide
OR
OCP + topical retinoid + topical antimicrobial + benzoyl peroxide

163
Q

What antibiotics are used in acne vulgaris?

A

Tetracyclines

Erythromycin

164
Q

What are the additional considerations with isotretinoin treatment?

A

Teratogenic - monitor

165
Q

What are the differentials for acne vulgaris?

A

Folliculitis
Rosacea
Acneiform eruptions

166
Q

What are the complications of acne vulgaris?

A

Depression/anxiety/suicide
Hyperpigmentation
Scarring

167
Q

What is acne fulminans?

A

Severe form

Fever, arthralgia, myalgia, hepatosplenomegaly, osteolytic bone lesion

168
Q

What is the prognosis of acne vulgaris?

A

Usually improved after adolescence

Severe lesions may leave scarring

169
Q

How can acne vulgaris be prevented?

A

Secondary - good skin care

170
Q

Define rosacea

A

Common inflammatory facial rash with papules and pustules on a background of erythema, most commonly occurring in mid-adult life

171
Q

What are the risk factors for rosacea?

A

Female
Prolonged steroid use
Light skin type
Exposure to triggers - hot showers, temperature extremes, sunlight, alcohol, emotional stress

172
Q

What is the aetiology of rosacea?

A

Unknown

May be triggered by demodex folliculorum mite

173
Q

What is seen on examination of rosacea?

A 
Flushing/fixed erythema
Inflammatory papules and pustules 
Convexities of face affected 
Telangiectasia, rough skin, rhinophyma 
Irritated eyes
174
Q

How is rosacea investigated?

A

Clinical diagnosis

Skin biopsy

175
Q

How is rosacea managed?

A

Supportive
Inflammation - metronidazole/azelaic cream with intermittent oral tetracyclines as required
Erythema - topical brimonidine, vascular laser therapy

176
Q

What are the differentials for rosacea?

A

Seborrhoeic/contact dermatitis
SLE
Dermatomyositis
Acne vulgaris

177
Q

What are the complications of rosacea?

A

Ocular involvement - blepharitis, conjunctivitis

Sebaceous gland/soft tissue overgrowth (especially nose in men)

178
Q

What is the prognosis of rosacea?

A

Range of severity and response to treatment

179
Q

How can rosacea be prevented?

A

Secondary - avoid triggers, good skincare

Year 4 Medicine (2 decks)

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