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MRCP > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What occurs in psoriasis?

A

hyperproliferation of keratinocytes and inflammatory cell infiltration
T-cell mediated

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2
Q

What are the different types of psoriasis?

A

Guttate - raindrop lesions (usually following strep infection)
Scalp/seborrheic
Flexural
Pustular

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3
Q

Peak ages of psoriasis onset and common ethnicity?

A

15-25
50-60
Caucasians

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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)

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5
Q

What is Auspitz sign?

A

Scratching of the lesions removes scales and causes capillary bleeding

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6
Q

What percentage of patients with psoriasis also have nail changes and what are these?

A

50% have associated nail changes – pitting, onycholysis

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7
Q

Conditions associated with psoriasis?

A
  • Psoriatic arthritis
  • IBD
  • Coeliac disease
  • Uveitis
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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)

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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

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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

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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

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12
Q

Where is eczema most common?

A

More common on the face and flexor aspects in children

On the extensors in infants

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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

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14
Q

Triggers for eczema?

A

infection, allergens (detergents, house dust), sweating, heat, stress

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15
Q

Investigations for eczema?

A

RAST test – blood test to detect specific IgE Abs

Patch test – placed on the back

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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

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17
Q

Risks of topical steroids?

A

skin thinning, systemic absorption

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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

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19
Q

What causes acne?

A

Hormones

Contributing factors - sebum production, follicular keratinisation, bacterial colonisation

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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

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21
Q

Complications of acne?

A

Post-inflammatory hyperpigmentation, scarring, deformity, psychological and social effects

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22
Q

What causes acne rosacea?

A

Unknown cause

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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)

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24
Q

Management of acne rosacea?

A

Topical metronidazole
Systemic abx for more severe disease – oral tetracyclines
Laser therapy for prominent telangiectasia

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25
Q

Steroid ranking in terms of strength?

A

1) Hydrocortisone
2) Eumovate
3) Betnovate
4) Dermovate

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26
Q

Cause of seborrhoea dermatitis?

A

Caused by inflammatory reaction to normal skin fungus called Malassezia furfur

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27
Q

Presentation of seborrhoea dermatitis?

A

Eczematous lesions on scalp, periorbital, auricular and nasolabial folds
Otitis externa + blepharitis

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28
Q

Management of seborrhoea dermatitis?

A

For scalp
First-line: OTC shampoos containing zinc pyrithione (head + shoulders) and tar (Neutrogena T/Gel)
Second-line: Ketoconazole

Elsewhere
Ketoconazole, potentially topical steroids

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29
Q

What is the name of the mite that causes scabies?

A

Sarcoptes scabei

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30
Q

How many mites live in a host on average in scabies? And in crusted scabies?

A

5-15

Crusted - may be hundreds

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31
Q

How long after scabies infection does the itch start?

A

30 days

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32
Q

Investigations for scabies?

A

Can extract mites from burrows using a sharp needle
Ink test – to show burrow
Skin scrapings can be taken with a blunt scalpel blade

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33
Q

Management of scabies? And crusted scabies?

A

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

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34
Q

Three main groups of fungal infections?

A

Dermatophytes (tinea/ringworm)
Yeasts (candidiasis)
Moulds (aspergillus)

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35
Q

Four types of dermatophytosis?

A 
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)
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36
Q

Investigations for dermatophytosis?

A

Skin scrapings

Hair/nail clippings

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37
Q

Management of dermatophytosis?

A

Topical antifungal agent e.g. terbinafine cream
Oral antifungals e.g. itraconazole for severe/widespread/nail infections
Avoid topical steroids

Tx tinea corporis = fluconazole

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38
Q

If not responsive to ketoconazole, how to treat pityriasis versicolour?

A

PO itraconazole

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39
Q

What is a BCC?

A

A slow-growing, locally invasive malignant tumour of the epidermal keratinocytes, normally in older individuals

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40
Q

Risk factors for a BCC?

A 
UV exposure/Hx of frequent/severe sunburn in childhood
Skin type 1 (always burns, never tans)
Elderly males
Immunosuppression
Genetic predisposition
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41
Q

Four different types of BCC?

A

Nodular ©
Superficial - most common in young adults
Morphoeic - wax scar like plaques with instinguishable borders
Keratotic

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42
Q

Features of nodular BCC?

A

small, skin-coloured papule/nodule with surface telangiectasia, and a pearly rolled edge, the lesion may have a necrotic or ulcerated centre (rodent ulcer)

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43
Q

Management of BCC?

A

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

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44
Q

What is a SCC?

A

A locally invasive malignant tumour of the epidermal keratinocytes

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45
Q

RFs of SCC?

A 
Pre-malignant skin conditions
Chronic inflammation e.g. leg ulcers
Immunosuppression
Genetic predisposition
Exposure to psoralen UV-A
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46
Q

What to do if patient with organ transplant develop new lesions?

A

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

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47
Q

Presentation of SCC?

A 
Keratotic, ill-defined nodules which may ulcerate
They grow over weeks – months
Often tender
May be ‘non-healing ulcers’
Located on sun-exposed sites
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48
Q

Types of SCC?

A

Cutaneous horn – d/t excessive keratin production
Keratoacanthoma
Carcinoma cuniculatum – slow-growing warty tumour on the sole of the foot

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49
Q

Management of SCC?

A

Surgical excision
Mohs micrographic surgery
Radiotherapy – for large non-resectable tumours

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50
Q

What is a malignant melanoma?

A

invasive malignant tumour of the epidermal melanocytes which can metastasise

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51
Q

RFs for malignant melanoma?

A

UV exposure
Skin type 1
Hx of moles/atypical moles
FH of melanoma

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52
Q

Features of malignant melanomas?

A 
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

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53
Q

Four types of malignant melanoma?

A

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

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54
Q

Management of malignant melanoma?

A

Surgical excision
Radiotherapy may sometimes be useful
Chemo for metastatic disease

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55
Q

Prognosis of malignant melanoma?

A

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

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56
Q

What is bullous pemphigoid?

A

A blistering skin disorder affecting the elderly

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57
Q

Cause of bullous pemphigoid?

A

AutoAbs against hemidesmosomal protein BP180 and BP230 between the epidermis and the dermis causing a sub-epidermal split in the skin

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58
Q

Presentation of bulllous pemphigoid?

A

Tense, fluid-filled blisters on a red base
Often itchy
Usually affects the trunk/limbs, flexures
No mucosal involvement

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59
Q

Management of bullous pemphigoid?

A

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

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60
Q

What is pemphigus vulgaris?

A

A blistering skin disorder which usually affects the middle-aged

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61
Q

Cause of pemphigus vulgaris?

A

AutoAbs against desmoglein 3 within the epidermis causing an intra-epidermal split in the skin

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62
Q

Presentation of pemphigus vulgaris?

A

Flaccid, easily ruptured blisters forming erosions and crusts
Lesions are often painful, NOT itchy
Usually affects the mucosal areas

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63
Q

Management of pemphigus vulgaris?

A

Wound dressing where required, look out for signs of infection, good oral care
Oral therapies – high-dose oral steroids, immunosuppressive agents

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64
Q

Causes of lichen planus?

A

AI disorder – purple, pruritic, popular, polygonal rash
Genetic predisposition - FH association in 10% of cases
May be drug-induced e.g. quinine

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65
Q

Where is lichen planus most commonly found?

A

Forearms, wrists + legs

Can be found on oral mucosa

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66
Q

What is Whickham’s striae?

A

when the plaques are crossed by lacy white streaks in lichen planus

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67
Q

How to investigate for lichen planus?

A

Skin biopsy

68
Q

Management of lichen planus?

A

Corticosteroids

Oral steroids or immunosuppression

69
Q

Prognosis of lichen planus?

A

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
Q

Who normally gets LS?

A

Most common in women >50

Often a FH of LS or another AI disease

71
Q

What is molluscum contagiosum look like?

A

Pink/white pearly papules with central indention

Lesions appear in clusters

72
Q

How is molluscum contagiosum transmitted?

A

Close contact/towels and flannels

73
Q

How to treat molluscum contagiosum?

A

Self-limiting within 18 months

74
Q

When does a strawberry naevus peak in size?

A

Usually 6-9 months

75
Q

Potential complications of strawberry naevus?

A

mechanical e.g. obstructing visual fields/airway, bleeding, ulceration

76
Q

Treatment (if needed) for strawberry naevus?

A

Propranolol

77
Q

Where do you normally get venous ulcers?

A

Common over medial malleolus

78
Q

What may be in the PMH in someone who developed a venous ulcer?

A

Hx of venous disease e.g. varicose veins, DVT

79
Q

What might you see in venous ulcers?

A

melanin deposits (brown pigment), lipodermatosclerosis and atrophie blanche (white scarring with dilated capillaries)

80
Q

Investigations in venous ulcers?

A 
Clinical
Do ABPI (0.8-1) to make sure the patients arterial supply is good enough to allow compression
81
Q

Management of venous ulcers?

A

Compression bandaging

82
Q

Presentation fo arterial ulcer and where found?

A

Small, sharply defined deep ulcer
Necrotic base
Found on pressure/trauma sites e.g. pretibial, supramalleolar (usually lateral), distally (toes)

83
Q

What makes the pain worse in arterial vs venous ulcers?

A

Venous - worse on standing

Arterial - worse at night when legs elevated

84
Q

What may be in the PMH in someone who developed a arterial ulcer?

A

Atherosclerosis

85
Q

Investigations for arterial ulcer?

A

ABPI <0.8 (presence of arterial insufficiency)

Doppler studies and angiography

86
Q

Management of arterial ulcer?

A

Vascular reconstruction

Compression bandaging is CI

87
Q

What dies a neuropathic ulcer look/feel like?

A

Variable size + depth
Granulating base
OFTEN PAINLESS
Abnormal sensation

88
Q

Where neuropathic ulcers commonly found?

A

May be surrounded by or underneath a hyperkeratotic lesion (callus)
Common on pressure sites (soles, heel, toes, metatarsal heads)

89
Q

Investigation in neuropathic ulcer?

A

ABPI <0.8 implies neuroischaemic ulcer

X-ray to exclude osteomyelitis

90
Q

Management of neuropathic ulcer?

A

Wound debridement

Regular repositioning, appropriate footwear and good nutrition

91
Q

Risk behaviour for PAD?

A

SMOKING

92
Q

Three types of PAD?

A

Intermittent claudication
Critical limb ischaemia
Acute life-threatening ischaemia

93
Q

What may occur as a complication of longterm abx use in acne? And how to Tx?

A

Gram-negative folliculitis - high-dose oral trimethoprim is effective if this occurs

94
Q

Causes of lichenoid drug eruptions?

A

gold
quinine
thiazides

95
Q

What is the SE of minocycline (used in acne)?

A

Irreversible skin pigmentation

96
Q

When should you avoid giving tetracyclines as a treatment for acne?

A

avoided in pregnant or breastfeeding women and in children younger than 12 years of age

97
Q

Which drugs can exacerbate psoriasis?

A

B-blockers, lithium, antimalarials, NSAIDs, ACEi

98
Q

Which conditions might develop livedo reticularis?

A 
idiopathic (most common)
polyarteritis nodosa
SLE/APS
cryoglobulinaemia
Ehlers-Danlos Syndrome
homocystinuria
99
Q

What is pyoderma gangrenosum?

A

Rare, non-infectious inflammatory disorder

Rapidly enlarging, very painful ulcer

100
Q

Where do you most commonly see pyoderma gangrenosum?

A

Most commonly on the lower legs – often at site of minor injury (pathergy)

101
Q

Cause of pyoderma gangrenosum?

A

Idiopathic (50%)
IBD (10-15%)
Rheumatological – RA, SLE
Haematological condition

102
Q

Features of pyoderma gangrenosum?

A

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
Q

Management of pyoderma gangrenosum?

A

Oral steroids
Immunosuppressive therapy – ciclosporin + infliximab
Postpone surgery to avoid risking more pathergy

104
Q

What is scrofuloderma?

A

Breakdown of skin overlying a tuberculoid focus (usually infected LN)

105
Q

What are necrobiosis lipoidica diabeticorum?

A

shiny, painless areas of yellow/red skin typically on the shin of diabetics
often associated with telangiectasia

106
Q

Organism that causes erysipelas?

A

S. pyogenes

107
Q

Features of erysipelas?

A

Abrupt onset painful erythema
Marked swelling
Systemic symptoms

108
Q

Management of erysipelas?

A

Penicillin
Erythromycin if allergic
Usually for 10-14 days

109
Q

Sedating antihistamine?

A

Chlorphenamine

110
Q

Non-sedating antihistamines?

A

loratidine
cetirizine
LORRYtadine - LEAST sedating of the two

111
Q

SE of retinoids?

A 
Tetrogenic
Dry skin ©
Low mood
Raised triglycerides
Hair thinning
Photosensitivity
112
Q

Why should you not combine isotretinoin treatment with tetracyclines?

A

Intracranial HTN

113
Q

What does hypertrichosis mean?

A

Androgen-independent hair growth

114
Q

What can cause SJS?

A

SANA

Sulphonamides/penicillins
Anticonvulsants - lamotrigine, carbamazepine, phenytoin
NSAIDs
Allopurinol

115
Q

How to manage SJS?

A

Admit to hospital for conservative management

First-line: IVIg if needed, then immunosuppressants

116
Q

What is Toxic Epidermal Necrosis (TEN)?

A

Extreme version of SJS

Characterised by extensive skin and mucosal necrosis + systemic toxicity

117
Q

What would you see on histology in TEN?

A

full-thickness epidermal necrosis with subepidermal detachment

118
Q

What is Nikolsky’s sign?

A

epidermis separates with mild lateral pressure

119
Q

Mortality in SJS and TEN?

A

Mortality – 5-12% with SJS

>30% with TEN

120
Q

Which cell type is predominantly involved in SJS/TEN?

A

T cell

121
Q

What causes acanthosis nigricans?

A

T2 DM, GI Ca, PCOS, obesity
Endocrine conditions – acromegaly, cushings, hypothyroidism
Drugs – cOCP, nicotinic acid

122
Q

What is the pathophysiology of acanthosis nigricans?

A

Insulin resistance -> hyperinsulinaemia -> stimulation of keratinocytes/fibroblast proliferation via IGF-receptor 1

123
Q

What are the symptoms of acanthosis nigricans?

A

Symmetrical, brown, velvety plaques – often found on neck, axilla + groin

124
Q

Causes of erythema nodosum?

A 
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
Q

What is Erythema gyratum repens associated with?

A

Swirly lines across skin, gyrating - ‘wood-grain’ appearance

Paraneoplastic - associated with lung cancer

126
Q

What type of hypersensitivity reaction is associated with scabies?

A

Delayed T4

127
Q

In which conditions can you see Koebner’s phenomenon?

A 
Psoriasis
Vitiligo
Warts
Lichen planus + sclerosis
Molluscum contagiosum
128
Q

Causes of non-scarring alopecia?

A 
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
Q

What is hyperhidrosis?

A

Excessive sweating

130
Q

How to treat hyperhidrosis?

A

Topical aluminium chloride SE: skin irritation
Iontophoresis (electrical current) - useful if palmar/plantar/axillary hyperhidrosis
Botox: axillary symptoms
Surgery - endoscopic transthoracic sympathectomy

131
Q

What causes pityriasis rosea?

A

HHV-7

132
Q

What are the features of pityriasis rosea?

A

May be history of recent viral illness
Herald patch (usually on trunk)
Erythematous, oval, scaly patches – ‘fir-tree’ appearance

133
Q

Management of pityriasis rosea?

A

Self-limiting – disappears after 6-12 weeks

134
Q

What are the features of zinc deficiency?

A 
Perioral dermatitis
Acrodermatitis
Alopecia
Short stature
Hepatosplenomegaly
Geophagia (ingesting clay)
Cognitive impairment
135
Q

What are the symptoms of selenium deficiency?

A

Fatigue, hair loss, weight gain, joint and muscle pain.

136
Q

What is Onychomycosis and what causes it?

A

Fungal nail infection
dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
yeasts - such as Candida
non-dermatophyte moulds

137
Q

Skin rashes associated with TB?

A

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
Q

What skin condition are patients at risk of after recurrent Erythema ab igne?

A

SCC

139
Q

What malignancy is associated with necrolytic migratory erythema?

A

Glucagonoma

140
Q

What is the most common malignancy to affect the lower lip?

A

SCC

141
Q

What is associated with yellow nail syndrome?

A

congenital lymphoedema
pleural effusions
bronchiectasis
chronic sinus infections

142
Q

How to treat vitiligo?

A

Sun cream + make-up

Steroids early, may be a role for topical tacrolimus and phototherapy

143
Q

Which cells are lost in vitiligo?

A

Melanocytes

144
Q

Which Ig would you see on biopsy in dermatitis herpetiformis?

A

IgA deposition in the dermis

145
Q

What are actinic keratoses?

A

Premalignant skin lesions that develops as a consequence of chronic sun exposure

146
Q

What is the management of actinic keratoses?

A 
Sun cream
Fluorouracil cream – 2-3 weeks
Topical diclofenac – if mild
Cryotherapy
Curettage and cautery
147
Q

What is a polymorphous light eruption?

A

A rash that develops when skin is exposed to sun

148
Q

Causes of Porphyria cutanea tarda?

A

Can be hereditary or occur in people with liver disease (excessive alcohol, hep B and C, haemochromatosis)
Due to defect in uroporphyrinogen decarboxylase

149
Q

Features of Porphyria cutanea tarda?

A

Photosensitive rash with blistering + skin fragility on face + dorsal aspect of hands
Hypertrichosis (hair growth)
Hyperpigmentation

150
Q

Investigations in Porphyria cutanea tarda?

A

Urine – elevated uroporphyrinogen + pink fluorescence of urine under Wood’s lamp
Serum iron ferritin level is used to guide therapy

151
Q

Management of Porphyria cutanea tarda?

A

Chloroquine

Venesection – if iron levels ok

152
Q

Drugs that cause hypertrichosis?

A

minoxidil, ciclosporin, diazoxide

153
Q

Which conditions are associated with seborrhoeic dermatitis?

A

Associated with HIV and parkinsons

154
Q

In who are keloid scars more common?

A

young, black, male adults

155
Q

What sort of incisions decrease the chance of keloid scarring?

A

Keloid scars are less likely if incisions are made along relaxed skin tension lines

156
Q

Treatment of keloid scarring?

A

early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required

157
Q

Inheritance pattern of hereditary haemorrhagic telangiectasia?

A

AD

158
Q

Features of hereditary haemorrhagic telangiectasia?

A 
Epistaxis: spontaneous, recurrent
Telangiectasis: Multiple
Visceral lesions: GI telangiectasia, pulmonary/hepatic/cerebral/spinal AV malformation
\+ FH
'Family VET'
159
Q

What is Necrobiosis lipoidica and what is it associated with?

A

Assoc with DM
shiny, painless areas of yellow/red/brown skin typically on the shin
often associated with surrounding telangiectasia

160
Q

What is Sweet’s syndrome associated with?

A

AML

161
Q

Skin conditions associated with DM?

A

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
Q

What do the following fungus lead to?
Trichophyton rubrum
Trichophyton verrucosum
Trichophyton tonsurans

A

Trichophyton rubrum -> fungal nail and tinea corporis
Trichophyton verrucosum -> tinea corporis
Trichophyton tonsurans -> tinea capitis

163
Q

Which type of melanoma is the most aggressive and metastasises early?

A

Nodular

164
Q

What is systemic mastocytosis?

A

A neoplastic proliferation of mast cells

165
Q

What is produced in systemic mastocytosis and what does this lead to?

A

Associated with increased histamine production -> leads to increased gastric acid production

166
Q

What are the features of systemic mastocytosis?

A

Urticaria pigmentosa (red-brown papules) – produces a wheal on irritation (Darier’s sign)
Flushing
Abdo pain
Monocytosis on blood film

167
Q

Diagnosis of systemic mastocytosis?

A

Raised serum tryptase levels

Urinary histamine

MRCP (14 decks)

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