Dermatology Flashcards

1
Q

What is the differential diagnosis for scarring alopecia?

A

Discoid lupus
Lichen planus
Tinea capitus

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2
Q

If a patient with DLE has negative autoantibodies what is their chance of developing SLE?

A

5% whereas 25% patients with systemic disease develop discoid lupus at some point

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3
Q

What are the potential side effects of chronic topical steroid applications

A

Telangiectasia
Skin breakdown
Ulceration

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4
Q

What is the management of discoid lupus?

A
Avoid sun
Sun protection
Stop smoking
Topical steroids
Topical tacrolimus
Antimalarials
Prednisolone
Azathioprine/mycophenolate/cyclophosphamide
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5
Q

How do you treat psoriasis?

A

Topical

  • soap substitutes eg aqueous cream
  • emollient
  • vitamin d analogues
  • salicylic acid
  • topical steroids
  • coal tar
  • dithranol

Photo (chemo) therapy

  • Narrow band UVB given for 6 weeks
  • Psoralen plas UVA (PUVA)- psoralen is applied topically or orally at time
  • Risk of carcinogenesis is a long term side effect

Systemic

  • methotrexate
  • retinoids
  • ciclosporin

Biologics
- etanercept/adalimumab/infliximab

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6
Q

What are the 6 clinical presentations of psoriasis?

A
  • chronic plaque psoriasis
  • Guttate psoriasis
  • Hyperkeratotic palmo-plantar psoriasis
  • flexural psoriasis
  • erythrodermic psoriasis (risk of sepsis and CV compromise)
  • Pustular psoriasis
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7
Q

What are the precipitating factors in psoriasis?

A

Physical trauma (Koebner phenomonen)
Infections (classically beta haemolytic strep)
Drugs (beta blockers, antimalarials, lithium, NSAIDs, steroids)
Stress
Alcohol
Tobacco
Climate

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8
Q

What are the two characteristic histological features seen in psoriasis?

A

Epidermal hyperplasia with squared off rete ridges

Inflammatory cell infiltrate in dermis and epidermis

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9
Q

How can you establish severity and functional status of patients with psoriasis?

A

PASI: The Psoriasis Area Severity Index: objective assessment of severity- looking at redness, scaling, thickness and area involved Max score 72

DLQI: Dermatology Life Quality Index- patient questionaire, subjective measures

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10
Q

How is neurofibromatosis inherited?

A

Autosomal dominant

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11
Q

WHat is the diagnostic criteria for neurofibromatosis type 1?

A

Presence of 2 or more of:

  • > 6 cafe au lait macules (>15mm in adult)
  • neurofibromas
  • Freckling in axilla or inguinal regions
  • > 2 Lisch nodules (eye brown spots)
  • Optic glioma
  • Distinctive osseus lesion- sphenoid dysplasia
  • 1st degree relative with NF1
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12
Q

What are the symptoms with NF1?

A

Skin lesions- neurofibromas can undergo sarcomatous changes- exicsions

Neurological

  • radicular pain (nerve compression due to neuromas)
  • Visual problems (secondary to optic gliomas)
  • Epilepsy (secondary CNS tumours)
  • History of brain tumours
  • Previous surgery (skin, nerves, spine, brain)
  • Learning difficulties

Bones
- lordosis, kyphosis, dislocations

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13
Q

How does type 2 neurofibromatosis classically present?

A

Hearing loss
Tinnitus
Balance problems

Result of unilateral or bilateral acoustic neuromas
Cutaneous features far less prominent

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14
Q

What are the diagnostic criteria of NF2?

A

Bilateral 8th CN masses
or 1st degree relative with NF2 and either unilateral 8th nerve mass or 2 of: neurofibroma, meningioma, glioma, schwannoma or juvenile posterior subcapsular lenticular opacity

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15
Q

Name 3 causes of hypertension associated with neurofibromatosis?

A

Renal artery stenosis
Phaeochromocytoma
Coarctation of aorta

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16
Q

On which chromosomes are the genes responsible for neurofibromatosis type 1 and 2?

A

NF1: chromosome 17
NF2: chromosome 22

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17
Q

What is the most common CNS tumour occuring in NF1?

A

OPtic glioma

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18
Q

What is Crowes sign?

A

Axillary freckling

19
Q

What is tuberous sclerosis?

A

Multisystem disorder characterised by the formation of harmartomas in many organs commonly the brain, skin and kidneys.

20
Q

How is tuberous sclerosis inherited and how does it present?

A

AD

Commonly presents in childhood with epilepsy and skin changes

21
Q

What are the features of tuberous sclerosis?

A
Ash leaf macules
Adenoma sebaceum (facial angiofibromas)
Shagreen patches over sacrum and back
Ungual fibromas
Skin tags
Cafe au lait spots

Renal

  • Renal angiomyolipoma- multiple benign
  • polycystic kidneys

Cognitive and behavioural problems

22
Q

What is vitiligo?

A

Acquired idiopathic disorder characterised by circumscribed de-pigmented macules and pacthcs. Functional melanocytes disappear from skin

23
Q

How do you manage vitiligo?

A
Psychological support
Camouflage
Suncream
Reversal: UVB, PUVA, tacrolimus, potent steroids
Depigmentation with bleaching creams
24
Q

What disorders are associated with vitiligo?

A
Autoimmune disorders
Strongest is thyroid disorders
- Pernicious anaemia
- Addisons disease
- Diabetes
- Alopecia
- Coeliac disease
25
Q

Is vitiligo familial?

A

Around 36% have a positive FH so a genetic component

26
Q

WHat is the histology of vitiligo?

A

Marked absence of melanocytes and melanin in epidermis

27
Q

Can you suggest any theories for the aetiology of vitiligo?

A

Autoimmune destruction due to antibodies against melanocytes

  • intrinsic defect in melanocytes
  • reduced melanocyte survival and dysregulation of melanocyte apoptosis
  • destruction of melanocytes by neurochemical substances
28
Q

What is pyoderma gangrenosum?

A

Uncommon, recurrent condition causing skin ulceration frequently assoc with underlying disease

29
Q

How do you treat pyoderma gangrenosum?

A
Bed rest
Topical steroids
High dose systemic steroids
systemic therapy eg ciclosporin or dapsone
Inflixumab
30
Q

What systemic disease are assoc with pyoderma gangrenosum?

A

around 50% have assoc condition

  • IBD
  • Crohns disease
  • Arthritis- RA
  • Haematological disease: AML, CML, hairy cell leukaemia, myelodysplasia, monoclonal gammopathy
31
Q

Apart from cutaneous sites, what other sites can be affected?

A

Mucous membranes and peristomal sites- sites of ileostomy and colostomy in UC and Crohns
Less commonly- vulva, penis, scrotum

32
Q

What are the four major clinical forms of pyoderma gangrenosum?

A

Ulcerative
Bullous
Pustular
Superficial granulomatous

33
Q

Is the histology in pyoderma gangrenosum specific?

A

No, non specific neutrophilic infiltration, haemorrhage and necrosis of epidermis

34
Q

What is necrobiosis lipodica?

A

Rare, chronic skin condition associated with diabetes mellitus. Granulomatous inflammation and fibrosis appears as yellow, atrophic skin lesions almost exclusively on shins.

35
Q

What proportion of patients with necrobiosis lipoidica have diabetes

A

Around 60%, occurs in both type 1 and type 2 but only 0.5% of patients with diabetes develop it.

36
Q

What are the other skin changes assoc with diabetes mellitus?

A

Infections: bacterial, fungal
Ulcers: arterial, neuropathic
Diabetic dermopathy: brown, scaly indented patches in skin
Diabetic bullae: blisters which heal spontaneously
Granuloma annular

37
Q

What are the signs of HHT?

A

Mutiple telangiectasia present on face and mouth
Pallor- anaemia
Nails- telangiectasia in nail bed
Visceral AVMs- pulmonary and hepatic bruits
- signs of high output cardiac failure due to left to right shunting between hepatic arteries and veins due to large AVM
- neurological sequalae

38
Q

What are the clinical criteria for diagnosis of HHT?

A

Curacao criteria:

  • epistaxis- spontaneous and recurrent
  • Telangiectasia: multiple and in characteristic sites
  • Visceral lesions: GI telangiectasia, pulmonary, hepatic, cerebral, spinal AVM
  • FH: 1st degree relative with HHT

3 criteria definite, 2 criteria=possible

39
Q

What are the complications of HHT?

A
GI haemorrhage: AVMs, angiodysplasia, telangiectasia
Epistaxis
Pulmonary AVM: haemoptysis
Iron def anaemia
Headache SAH
40
Q

What is porphyria cutanea tarda?

A

Caused by a deficiency of enzyme uroporphyrinogen decarboxylase (UROD) leading to accumulation of porphyrins in skin and resultant photo-induced dermatitis.
Characterised by bullae, milia and scarring over sun exposed sites.

41
Q

What are the pre-disposing factors in porphyria cutanea tarda?

A

Alcohol intake: high intake worsens conditions
History of hepatitis often assoc
History of liver problems eg haemochromatosis
Oestrogens that reduce UROD activity

42
Q

How do you diagnose porphyria cutanea tarda?

A

Urine examination: fluresces pink/coral under woods light
24hr urine uroporphyrins
skin biopsy
If diagnosis made then consider investigating for hepatitis, iron/ferritin levels and AFP

43
Q

How would you treat porphyria cutanea tarda?

A

Removal of contributing agents eg alcohol, oestrogen containing med
Sun avoidance
Phelbotomy (iron stores in liver inhibit UROD enzyme)
Anti-malarials- chloroquine