Dermatology Flashcards
1
Q
What occurs in psoriasis?
A
hyperproliferation of keratinocytes and inflammatory cell infiltration
T-cell mediated
2
Q
What are the different types of psoriasis?
A
Guttate - raindrop lesions (usually following strep infection)
Scalp/seborrheic
Flexural
Pustular
3
Q
Peak ages of psoriasis onset and common ethnicity?
A
15-25
50-60
Caucasians
4
Q
What are the contributing factors/possible cause of psoriasis? Phenomenom?
A
Genetic, immunological and environmental factors
May be precipitated by infection, drugs, stress, alcohol, trauma (Koebner
Phenomenom – plaques are more common at sites of skin injury, often linear lesions)
5
Q
What is Auspitz sign?
A
Scratching of the lesions removes scales and causes capillary bleeding
6
Q
What percentage of patients with psoriasis also have nail changes and what are these?
A
50% have associated nail changes – pitting, onycholysis
7
Q
Conditions associated with psoriasis?
A
- Psoriatic arthritis
- IBD
- Coeliac disease
- Uveitis
8
Q
Management of psoriasis in primary care?
A
General – avoid precipitating factors
Topical (for mild) – emollients
First-line – corticosteroids OD + vit D analogues OD e.g. calcipotriol, calcitriol -> reduces cell division and differentiation, can be used longterm
Second-line – vit D analogue BD
Third-line – corticosteroid BD or coal tar preparations (used for scalps sometimes e.g. shampoos, inhibits DNA synthesis)
9
Q
What are the maximum lengths of time to use steroids in psoriasis?
A
Very potent steroids – max 4 weeks at a time
Potent – max 8 weeks
10
Q
Management of psoriasis in secondary care?
A
Phototherapy (for extensive disease) e.g. UV-B and photochemotherapy (psoralen + UV-A)
Oral therapies (for severe/systemic) – methotrexate, retinoids (vit A derivative), ciclosporin, biologics
11
Q
Complications of psoriasis?
A
Erythroderma (red skin over 90% of body) – risk of infection, loss of heat and dehydration, dermatological emergency
Psoriatic arthropathy
Psychological and social impact
12
Q
Where is eczema most common?
A
More common on the face and flexor aspects in children
On the extensors in infants
13
Q
What causes eczema?
A
Not fully understood
Likely to be a primary genetic defect in skin barrier function
A mixture of type 1 and type 4 hypersensitivity
14
Q
Triggers for eczema?
A
infection, allergens (detergents, house dust), sweating, heat, stress
15
Q
Investigations for eczema?
A
RAST test – blood test to detect specific IgE Abs
Patch test – placed on the back
16
Q
Management of eczema?
A
General measures – avoid exacerbating agents, use emollients +/- bandages and bath oil/soap substitute
Topical therapies – topical steroids for flare-ups, topical immunomodulators can be used as steroid-sparing agents
Oral therapies – antihistamines (not just for itch, may help with hayfever season etc), abx (flucloxacillin) for secondary bacterial infections and antivirals (aciclovir) for secondary herpes infection
Phototherapy and immunosuppressants (pred, azathioprine, ciclosporin) for severe non-responsive cases
17
Q
Risks of topical steroids?
A
skin thinning, systemic absorption
18
Q
What is eczema herpeticum and how to treat?
A
Describes a severe primary skin infection by HSV1 or HSV2
More common in children with atopic eczema
LIFE-THREATENING
Admit, IV aciclovir
19
Q
What causes acne?
A
Hormones
Contributing factors - sebum production, follicular keratinisation, bacterial colonisation
20
Q
Treatment of acne?
A
Minimum 6 week treatment
• Topical therapies – benzoyl peroxide + abx, topical retinoids
• Oral therapies (should always be co-prescribed with a topical retinoid or BP) – oral abx (e.g. tetracyclines, erythromycin (preg), minocycline – SE: irreversible skin pigmentation), anti-androgens e.g. cOCP (for females)
• Oral retinoids
21
Q
Complications of acne?
A
Post-inflammatory hyperpigmentation, scarring, deformity, psychological and social effects
22
Q
What causes acne rosacea?
A
Unknown cause
23
Q
Presentation of acne rosacea?
A
Affects nose, cheeks, forehead
Flushing
Telangiectasia
Later, persistent erythema with papules + pustules
Rhinophyma (cauliflower like nose – my words)
24
Q
Management of acne rosacea?
A
Topical metronidazole
Systemic abx for more severe disease – oral tetracyclines
Laser therapy for prominent telangiectasia
25
Steroid ranking in terms of strength?
1) Hydrocortisone
2) Eumovate
3) Betnovate
4) Dermovate
26
Cause of seborrhoea dermatitis?
Caused by inflammatory reaction to normal skin fungus called Malassezia furfur
27
Presentation of seborrhoea dermatitis?
Eczematous lesions on scalp, periorbital, auricular and nasolabial folds
Otitis externa + blepharitis
28
Management of seborrhoea dermatitis?
For scalp
First-line: OTC shampoos containing zinc pyrithione (head + shoulders) and tar (Neutrogena T/Gel)
Second-line: Ketoconazole
Elsewhere
Ketoconazole, potentially topical steroids
29
What is the name of the mite that causes scabies?
Sarcoptes scabei
30
How many mites live in a host on average in scabies? And in crusted scabies?
5-15
| Crusted - may be hundreds
31
How long after scabies infection does the itch start?
30 days
32
Investigations for scabies?
Can extract mites from burrows using a sharp needle
Ink test – to show burrow
Skin scrapings can be taken with a blunt scalpel blade
33
Management of scabies? And crusted scabies?
Permethrin (applied all over at bedtime, repeat after one week, can remain itchy as mite debris has been burrowed quite deep into skin)
Malathion cream 2nd line
Wash all clothing/bed linin, treat close contacts
Pruritis persists for 4-6wks post eradication
Crusted scabies - Mx = ivermectin
34
Three main groups of fungal infections?
Dermatophytes (tinea/ringworm)
Yeasts (candidiasis)
Moulds (aspergillus)
35
Four types of dermatophytosis?
```
Tinea corporis - ringworm (infection on the trunk/limbs)
Tinea cruris (infection of the groin/natal cleft)
Tinea pedis (athlete’s foot)
Tinea capitis (scalp ringworm)
```
36
Investigations for dermatophytosis?
Skin scrapings
| Hair/nail clippings
37
Management of dermatophytosis?
Topical antifungal agent e.g. terbinafine cream
Oral antifungals e.g. itraconazole for severe/widespread/nail infections
Avoid topical steroids
Tx tinea corporis = fluconazole
38
If not responsive to ketoconazole, how to treat pityriasis versicolour?
PO itraconazole
39
What is a BCC?
A slow-growing, locally invasive malignant tumour of the epidermal keratinocytes, normally in older individuals
40
Risk factors for a BCC?
```
UV exposure/Hx of frequent/severe sunburn in childhood
Skin type 1 (always burns, never tans)
Elderly males
Immunosuppression
Genetic predisposition
```
41
Four different types of BCC?
Nodular ©
Superficial - most common in young adults
Morphoeic - wax scar like plaques with instinguishable borders
Keratotic
42
Features of nodular BCC?
small, skin-coloured papule/nodule with surface telangiectasia, and a pearly rolled edge, the lesion may have a necrotic or ulcerated centre (rodent ulcer)
43
Management of BCC?
Surgical excision – this allows histological examination of the tumour and margins
o (Mohs micrographically controlled excision – carefully examining the excised tissue under the microscope to ensure complete excision)
Curettage and cautery/cryotherapy – suitable for small superficial BCCs
Topical treatment (e.g. imiquimod cream) for small/low-risk lesions
Radiotherapy – where surgery is not appropriate
Topical photodynamic therapy – for small, low-risk BCCs
44
What is a SCC?
A locally invasive malignant tumour of the epidermal keratinocytes
45
RFs of SCC?
```
Pre-malignant skin conditions
Chronic inflammation e.g. leg ulcers
Immunosuppression
Genetic predisposition
Exposure to psoralen UV-A
```
46
What to do if patient with organ transplant develop new lesions?
NICE advises all patients who have received organ transplants are referred urgently to a dermatologist if they present with any new or growing skin lesions
47
Presentation of SCC?
```
Keratotic, ill-defined nodules which may ulcerate
They grow over weeks – months
Often tender
May be ‘non-healing ulcers’
Located on sun-exposed sites
```
48
Types of SCC?
Cutaneous horn – d/t excessive keratin production
Keratoacanthoma
Carcinoma cuniculatum – slow-growing warty tumour on the sole of the foot
49
Management of SCC?
Surgical excision
Mohs micrographic surgery
Radiotherapy – for large non-resectable tumours
50
What is a malignant melanoma?
invasive malignant tumour of the epidermal melanocytes which can metastasise
51
RFs for malignant melanoma?
UV exposure
Skin type 1
Hx of moles/atypical moles
FH of melanoma
52
Features of malignant melanomas?
```
ABCDE symptoms
Asymmetrical shape
Border irregularity
Colour irregularity
Diameter >6mm
Evolution of lesion (change in size/shape)
Symptoms – bleeding, itching
```
More common on the legs in women and trunk in men
53
Four types of malignant melanoma?
o Superficial spreading melanoma (70%) – common on trunk/
- limbs in young/middle-aged adults, related to intermittent high-intensity UV exposure
o Nodular melanoma – common on sun exposed skin in young/middle-aged adults, related to intermittent high-intensity UV
- aggressive, mets early
o Lentigo maligna melanoma – common on the face in the elderly, related to long-term cumulative UV exposure
o Acral lentiginous melanoma – common on the palms, soles and nail beds in elderly population, no clear relation to UV
54
Management of malignant melanoma?
Surgical excision
Radiotherapy may sometimes be useful
Chemo for metastatic disease
55
Prognosis of malignant melanoma?
Recurrence of melanoma based on Breslow thickness (thickness of tumour) – the thicker it is, the more likely to recur
5 year survival based on TNM classification
56
What is bullous pemphigoid?
A blistering skin disorder affecting the elderly
57
Cause of bullous pemphigoid?
AutoAbs against hemidesmosomal protein BP180 and BP230 between the epidermis and the dermis causing a sub-epidermal split in the skin
58
Presentation of bulllous pemphigoid?
Tense, fluid-filled blisters on a red base
Often itchy
Usually affects the trunk/limbs, flexures
No mucosal involvement
59
Management of bullous pemphigoid?
Wound dressings where required, look out for signs of infection
Topical steroids for localised disease
Oral therapies for widespread disease e.g. oral steroids, combination of oral tetracycline + nicotinamide, immunosuppressive agents
60
What is pemphigus vulgaris?
A blistering skin disorder which usually affects the middle-aged
61
Cause of pemphigus vulgaris?
AutoAbs against desmoglein 3 within the epidermis causing an intra-epidermal split in the skin
62
Presentation of pemphigus vulgaris?
Flaccid, easily ruptured blisters forming erosions and crusts
Lesions are often painful, NOT itchy
Usually affects the mucosal areas
63
Management of pemphigus vulgaris?
Wound dressing where required, look out for signs of infection, good oral care
Oral therapies – high-dose oral steroids, immunosuppressive agents
64
Causes of lichen planus?
AI disorder – purple, pruritic, popular, polygonal rash
Genetic predisposition - FH association in 10% of cases
May be drug-induced e.g. quinine
65
Where is lichen planus most commonly found?
Forearms, wrists + legs
| Can be found on oral mucosa
66
What is Whickham's striae?
when the plaques are crossed by lacy white streaks in lichen planus
67
How to investigate for lichen planus?
Skin biopsy
68
Management of lichen planus?
Corticosteroids
| Oral steroids or immunosuppression
69
Prognosis of lichen planus?
Cutaneous lichen planus tends to clear within a couple of years for most people
Mucosal can persist for longer
May recur at a later date
Scarring is permanent, including balding of the scalp
70
Who normally gets LS?
Most common in women >50
| Often a FH of LS or another AI disease
71
What is molluscum contagiosum look like?
Pink/white pearly papules with central indention
| Lesions appear in clusters
72
How is molluscum contagiosum transmitted?
Close contact/towels and flannels
73
How to treat molluscum contagiosum?
Self-limiting within 18 months
74
When does a strawberry naevus peak in size?
Usually 6-9 months
75
Potential complications of strawberry naevus?
mechanical e.g. obstructing visual fields/airway, bleeding, ulceration
76
Treatment (if needed) for strawberry naevus?
Propranolol
77
Where do you normally get venous ulcers?
Common over medial malleolus
78
What may be in the PMH in someone who developed a venous ulcer?
Hx of venous disease e.g. varicose veins, DVT
79
What might you see in venous ulcers?
melanin deposits (brown pigment), lipodermatosclerosis and atrophie blanche (white scarring with dilated capillaries)
80
Investigations in venous ulcers?
```
Clinical
Do ABPI (0.8-1) to make sure the patients arterial supply is good enough to allow compression
```
81
Management of venous ulcers?
Compression bandaging
82
Presentation fo arterial ulcer and where found?
Small, sharply defined deep ulcer
Necrotic base
Found on pressure/trauma sites e.g. pretibial, supramalleolar (usually lateral), distally (toes)
83
What makes the pain worse in arterial vs venous ulcers?
Venous - worse on standing
| Arterial - worse at night when legs elevated
84
What may be in the PMH in someone who developed a arterial ulcer?
Atherosclerosis
85
Investigations for arterial ulcer?
ABPI <0.8 (presence of arterial insufficiency)
| Doppler studies and angiography
86
Management of arterial ulcer?
Vascular reconstruction
| Compression bandaging is CI
87
What dies a neuropathic ulcer look/feel like?
Variable size + depth
Granulating base
OFTEN PAINLESS
Abnormal sensation
88
Where neuropathic ulcers commonly found?
May be surrounded by or underneath a hyperkeratotic lesion (callus)
Common on pressure sites (soles, heel, toes, metatarsal heads)
89
Investigation in neuropathic ulcer?
ABPI <0.8 implies neuroischaemic ulcer
| X-ray to exclude osteomyelitis
90
Management of neuropathic ulcer?
Wound debridement
| Regular repositioning, appropriate footwear and good nutrition
91
Risk behaviour for PAD?
SMOKING
92
Three types of PAD?
Intermittent claudication
Critical limb ischaemia
Acute life-threatening ischaemia
93
What may occur as a complication of longterm abx use in acne? And how to Tx?
Gram-negative folliculitis - high-dose oral trimethoprim is effective if this occurs
94
Causes of lichenoid drug eruptions?
gold
quinine
thiazides
95
What is the SE of minocycline (used in acne)?
Irreversible skin pigmentation
96
When should you avoid giving tetracyclines as a treatment for acne?
avoided in pregnant or breastfeeding women and in children younger than 12 years of age
97
Which drugs can exacerbate psoriasis?
B-blockers, lithium, antimalarials, NSAIDs, ACEi
98
Which conditions might develop livedo reticularis?
```
idiopathic (most common)
polyarteritis nodosa
SLE/APS
cryoglobulinaemia
Ehlers-Danlos Syndrome
homocystinuria
```
99
What is pyoderma gangrenosum?
Rare, non-infectious inflammatory disorder
| Rapidly enlarging, very painful ulcer
100
Where do you most commonly see pyoderma gangrenosum?
Most commonly on the lower legs – often at site of minor injury (pathergy)
101
Cause of pyoderma gangrenosum?
Idiopathic (50%)
IBD (10-15%)
Rheumatological – RA, SLE
Haematological condition
102
Features of pyoderma gangrenosum?
Sudden formation of small pustule
Skin breaks down to form a painful deep ulcer (purple undermined edge)
May be systemic symptoms
May form around a stoma site in someone with IBD
103
Management of pyoderma gangrenosum?
Oral steroids
Immunosuppressive therapy – ciclosporin + infliximab
Postpone surgery to avoid risking more pathergy
104
What is scrofuloderma?
Breakdown of skin overlying a tuberculoid focus (usually infected LN)
105
What are necrobiosis lipoidica diabeticorum?
shiny, painless areas of yellow/red skin typically on the shin of diabetics
often associated with telangiectasia
106
Organism that causes erysipelas?
S. pyogenes
107
Features of erysipelas?
Abrupt onset painful erythema
Marked swelling
Systemic symptoms
108
Management of erysipelas?
Penicillin
Erythromycin if allergic
Usually for 10-14 days
109
Sedating antihistamine?
Chlorphenamine
110
Non-sedating antihistamines?
loratidine
cetirizine
LORRYtadine - LEAST sedating of the two
111
SE of retinoids?
```
Tetrogenic
Dry skin ©
Low mood
Raised triglycerides
Hair thinning
Photosensitivity
```
112
Why should you not combine isotretinoin treatment with tetracyclines?
Intracranial HTN
113
What does hypertrichosis mean?
Androgen-independent hair growth
114
What can cause SJS?
SANA
Sulphonamides/penicillins
Anticonvulsants - lamotrigine, carbamazepine, phenytoin
NSAIDs
Allopurinol
115
How to manage SJS?
Admit to hospital for conservative management
| First-line: IVIg if needed, then immunosuppressants
116
What is Toxic Epidermal Necrosis (TEN)?
Extreme version of SJS
| Characterised by extensive skin and mucosal necrosis + systemic toxicity
117
What would you see on histology in TEN?
full-thickness epidermal necrosis with subepidermal detachment
118
What is Nikolsky’s sign?
epidermis separates with mild lateral pressure
119
Mortality in SJS and TEN?
Mortality – 5-12% with SJS
| >30% with TEN
120
Which cell type is predominantly involved in SJS/TEN?
T cell
121
What causes acanthosis nigricans?
T2 DM, GI Ca, PCOS, obesity
Endocrine conditions – acromegaly, cushings, hypothyroidism
Drugs – cOCP, nicotinic acid
122
What is the pathophysiology of acanthosis nigricans?
Insulin resistance -> hyperinsulinaemia -> stimulation of keratinocytes/fibroblast proliferation via IGF-receptor 1
123
What are the symptoms of acanthosis nigricans?
Symmetrical, brown, velvety plaques – often found on neck, axilla + groin
124
Causes of erythema nodosum?
```
NODOSUM
NO: NO causes in 80% of cases
D : Drugs (sulfonamides; amoxicillin)
O : Oral contraceptive pills
S : Sarcoidosis/ Tuberculosis
U : Ulcerative colitis; Crohn's disease; Behcet disease
M: Micro
Viral : HSV; EBV; Hep B; Hep C
Bacterial: campylobacter; salmonella; streptococci; Brucellosis
Parasite : Amoebiasis; Giardiasis
```
125
What is Erythema gyratum repens associated with?
Swirly lines across skin, gyrating - 'wood-grain' appearance
| Paraneoplastic - associated with lung cancer
126
What type of hypersensitivity reaction is associated with scabies?
Delayed T4
127
In which conditions can you see Koebner's phenomenon?
```
Psoriasis
Vitiligo
Warts
Lichen planus + sclerosis
Molluscum contagiosum
```
128
Causes of non-scarring alopecia?
```
Male pattern baldness
Drugs: cytotoxic drugs, carbimazole, oral Con pill, colchicine, anti-Coagulant (heparin)
Alopecia areata (autoimmune)
Telogen effluvium (when stressed)
Iron/zinc deficiency
```
129
What is hyperhidrosis?
Excessive sweating
130
How to treat hyperhidrosis?
Topical aluminium chloride SE: skin irritation
Iontophoresis (electrical current) - useful if palmar/plantar/axillary hyperhidrosis
Botox: axillary symptoms
Surgery - endoscopic transthoracic sympathectomy
131
What causes pityriasis rosea?
HHV-7
132
What are the features of pityriasis rosea?
May be history of recent viral illness
Herald patch (usually on trunk)
Erythematous, oval, scaly patches – ‘fir-tree’ appearance
133
Management of pityriasis rosea?
Self-limiting – disappears after 6-12 weeks
134
What are the features of zinc deficiency?
```
Perioral dermatitis
Acrodermatitis
Alopecia
Short stature
Hepatosplenomegaly
Geophagia (ingesting clay)
Cognitive impairment
```
135
What are the symptoms of selenium deficiency?
Fatigue, hair loss, weight gain, joint and muscle pain.
136
What is Onychomycosis and what causes it?
Fungal nail infection
dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
yeasts - such as Candida
non-dermatophyte moulds
137
Skin rashes associated with TB?
lupus vulgaris (accounts for 50% of cases) - seen in Indian, cutaneous TB
erythema nodosum
scarring alopecia
scrofuloderma
verrucosa cutis - can occur after second infection in a previously infected individual
gumma
138
What skin condition are patients at risk of after recurrent Erythema ab igne?
SCC
139
What malignancy is associated with necrolytic migratory erythema?
Glucagonoma
140
What is the most common malignancy to affect the lower lip?
SCC
141
What is associated with yellow nail syndrome?
congenital lymphoedema
pleural effusions
bronchiectasis
chronic sinus infections
142
How to treat vitiligo?
Sun cream + make-up
| Steroids early, may be a role for topical tacrolimus and phototherapy
143
Which cells are lost in vitiligo?
Melanocytes
144
Which Ig would you see on biopsy in dermatitis herpetiformis?
IgA deposition in the dermis
145
What are actinic keratoses?
Premalignant skin lesions that develops as a consequence of chronic sun exposure
146
What is the management of actinic keratoses?
```
Sun cream
Fluorouracil cream – 2-3 weeks
Topical diclofenac – if mild
Cryotherapy
Curettage and cautery
```
147
What is a polymorphous light eruption?
A rash that develops when skin is exposed to sun
148
Causes of Porphyria cutanea tarda?
Can be hereditary or occur in people with liver disease (excessive alcohol, hep B and C, haemochromatosis)
Due to defect in uroporphyrinogen decarboxylase
149
Features of Porphyria cutanea tarda?
Photosensitive rash with blistering + skin fragility on face + dorsal aspect of hands
Hypertrichosis (hair growth)
Hyperpigmentation
150
Investigations in Porphyria cutanea tarda?
Urine – elevated uroporphyrinogen + pink fluorescence of urine under Wood’s lamp
Serum iron ferritin level is used to guide therapy
151
Management of Porphyria cutanea tarda?
Chloroquine
| Venesection – if iron levels ok
152
Drugs that cause hypertrichosis?
minoxidil, ciclosporin, diazoxide
153
Which conditions are associated with seborrhoeic dermatitis?
Associated with HIV and parkinsons
154
In who are keloid scars more common?
young, black, male adults
155
What sort of incisions decrease the chance of keloid scarring?
Keloid scars are less likely if incisions are made along relaxed skin tension lines
156
Treatment of keloid scarring?
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required
157
Inheritance pattern of hereditary haemorrhagic telangiectasia?
AD
158
Features of hereditary haemorrhagic telangiectasia?
```
Epistaxis: spontaneous, recurrent
Telangiectasis: Multiple
Visceral lesions: GI telangiectasia, pulmonary/hepatic/cerebral/spinal AV malformation
+ FH
'Family VET'
```
159
What is Necrobiosis lipoidica and what is it associated with?
Assoc with DM
shiny, painless areas of yellow/red/brown skin typically on the shin
often associated with surrounding telangiectasia
160
What is Sweet's syndrome associated with?
AML
161
Skin conditions associated with DM?
Granuloma annulare
Necrobiosis lipoidica
Vitiligo
Lipatrophy
Skin rxns in DM are LOVINNG:
LipOatrophy
Vitiligo
Infectious (strep, candida)
Necrobiosis lipoidica diabeticorum (shiny, painless, yellow/brown, surrounding telangiectasia)
Neuropathic ulcers
Granuloma annulare (hyperpigmented, centrally depressed)
162
What do the following fungus lead to?
Trichophyton rubrum
Trichophyton verrucosum
Trichophyton tonsurans
Trichophyton rubrum -> fungal nail and tinea corporis
Trichophyton verrucosum -> tinea corporis
Trichophyton tonsurans -> tinea capitis
163
Which type of melanoma is the most aggressive and metastasises early?
Nodular
164
What is systemic mastocytosis?
A neoplastic proliferation of mast cells
165
What is produced in systemic mastocytosis and what does this lead to?
Associated with increased histamine production -> leads to increased gastric acid production
166
What are the features of systemic mastocytosis?
Urticaria pigmentosa (red-brown papules) – produces a wheal on irritation (Darier’s sign)
Flushing
Abdo pain
Monocytosis on blood film
167
Diagnosis of systemic mastocytosis?
Raised serum tryptase levels
| Urinary histamine
