Derm Flashcards
(85 cards)
1
Q
What is lichen planus?
A
Lichen planus is a skin disorder of unknown aetiology, most probably being immune-mediated.
2
Q
What are the common features of lichen planus?
A
Itchy, papular rash most common on the palms, soles, genitalia, and flexor surfaces of arms.
Planus: purple, pruritic, papular, polygonal rash on flexor surfaces, wickham’s striae over surface
3
Q
What is the characteristic shape of the rash in lichen planus?
A
The rash is often polygonal in shape, with a ‘white-lines’ pattern on the surface (Wickham’s striae).
4
Q
What is the Koebner phenomenon?
A
(new skin lesions appearing at the site of trauma).
5
Q
What percentage of patients experience oral involvement in lichen planus?
A
Oral involvement occurs in around 50% of patients.
6
Q
What does oral involvement in lichen planus typically look like?
A
Typically presents as a white-lace pattern on the buccal mucosa.
7
Q
What are the nail changes associated with lichen planus?
A
Nail changes include thinning of the nail plate and longitudinal ridging.
8
Q
What are the causes of lichenoid drug eruptions?
A
Gold, quinine, and thiazides.
9
Q
What is the mainstay of treatment for lichenoid drug eruptions?
A
Potent topical steroids.
10
Q
What is recommended for oral lichen planus?
A
Benzydamine mouthwash or spray.
11
Q
What may extensive lichen planus require?
A
Oral steroids or immunosuppression.
12
Q
What is dermatitis herpetiformis?
A
An autoimmune blistering skin disorder associated with coeliac disease.
13
Q
What causes dermatitis herpetiformis?
A
Deposition of IgA in the dermis.
14
Q
What percentage of patients with dermatitis herpetiformis show small bowel biopsy findings consistent with gluten-sensitive enteropathy?
A
More than 90%.
15
Q
What are the features of dermatitis herpetiformis?
A
Itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks).
16
Q
How is dermatitis herpetiformis diagnosed?
A
Skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis.
17
Q
What is the management for dermatitis herpetiformis?
A
Gluten-free diet and dapsone.
18
Q
What are keloid scars?
A
Keloid scars are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound.
19
Q
What are the predisposing factors for keloid scars?
A
- Dark skin
- Young adults
- Rare in the elderly
20
Q
What are the common sites for keloid scars?
A
Common sites for keloid scars, in order of decreasing frequency, are sternum, shoulder, neck, face, extensor surface of limbs, and trunk.
21
Q
How can the likelihood of keloid scars be reduced?
A
Keloid scars are less likely if incisions are made along relaxed skin tension lines.
22
Q
What is the treatment for early keloids?
A
Early keloids may be treated with intra-lesional steroids, such as triamcinolone.
Excision sometimes required, careful consideration needed as potential create further keloid scarring
23
Q
What are Langer lines?
A
Langer lines were historically used to determine the optimal incision line but have been shown to produce worse cosmetic results than when following skin tension lines.
24
Q
What is Porphyria cutanea tarda?
A
Porphyria cutanea tarda is the most common hepatic porphyria, due to an inherited defect in uroporphyrinogen decarboxylase or caused by hepatocyte damage.
25
What are common causes of Porphyria cutanea tarda?
* Alcohol
* Hepatitis C
* Oestrogen
26
What are the classical features of Porphyria cutanea tarda?
* Photosensitive rash
* Blistering
* Skin fragility on the face and dorsal aspect of hands
* Hypertrichosis
*Hyperpigmentation.
27
What urine findings are associated with Porphyria cutanea tarda?
Urine shows elevated uroporphyrinogen and pink fluorescence under Wood's lamp.
28
What serum level is used to guide therapy in Porphyria cutanea tarda?
Serum iron ferritin level is used to guide therapy.
29
What is the management for Porphyria cutanea tarda?
Management includes chloroquine and venesection, preferred if iron ferritin is above 600 ng/ml.
30
What is the prevalence of psoriasis?
Around 2%
## Footnote
Psoriasis is a common chronic skin disorder.
31
What are the typical presentations of psoriasis?
Red, scaly patches on the skin
## Footnote
These patches are characteristic of the condition.
32
What increased risks are associated with psoriasis?
Increased risk of arthritis and cardiovascular disease
## Footnote
Patients with psoriasis face higher health risks.
33
What is the pathophysiology of psoriasis?
Multifactorial and not yet fully understood
## Footnote
The exact mechanisms contributing to psoriasis are complex.
34
Which genetic factors are associated with psoriasis?
HLA-B13, -B17, and -Cw6
## Footnote
Genetic predisposition plays a significant role in psoriasis.
35
What is the concordance rate of psoriasis in identical twins?
70%
## Footnote
This indicates a strong genetic component to the disease.
36
What immunological factor stimulates keratinocyte proliferation in psoriasis?
Abnormal T cell activity
## Footnote
This is a key aspect of the disease's pathophysiology.
37
Which novel group of T helper cells is involved in psoriasis?
Th17
## Footnote
Th17 cells produce IL-17 and are a distinct subset in T-effector cells.
38
What environmental factors can affect psoriasis?
Worsened by skin trauma and stress; triggered by streptococcal infection; improved by sunlight
## Footnote
Environmental influences can significantly impact the condition.
39
What is the most common subtype of psoriasis?
Plaque psoriasis
## Footnote
This subtype is characterized by well-demarcated red, scaly patches.
40
How does flexural psoriasis differ from plaque psoriasis?
The skin is smooth in flexural psoriasis
## Footnote
This subtype presents differently than the typical plaque form.
41
What triggers guttate psoriasis?
Frequently triggered by a streptococcal infection
## Footnote
This subtype often appears as transient red, teardrop lesions.
42
Where does pustular psoriasis commonly occur?
On the palms and soles
## Footnote
This form of psoriasis has a specific location of occurrence.
43
What are common nail signs associated with psoriasis?
Pitting and onycholysis
## Footnote
Nail involvement is a notable feature of the condition.
44
What are the complications of psoriasis
* Psoriatic arthropathy (~ 10%)
* Metabolic syndrome
* Cardiovascular disease
* Venous thromboembolism
* Psychological distress
## Footnote
Psoriasis is linked to several serious health conditions.
45
What is the overall stepwise approach for managing chronic plaque psoriasis in primary care (NICE)?
Regular **emollients** to reduce scale loss and pruritus.
First-line:
* **potent corticosteroid** OD + **vitamin D analogue** OD
Second-line (no improvement after 8/52):
* **vitamin D analogue** twice daily.
Third-line (no improvement after 8–12 weeks):
* potent **corticosteroid** **BD** for up to 4/52, or
* **coal tar preparation**
* short-acting **dithranol**
46
What are the first-line topical agents for initial treatment of chronic plaque psoriasis?
Potent topical corticosteroid, applied once daily.
Vitamin D analogue, applied once daily.
Apply separately (one in the morning; one in the evening).
47
When should second-line topical therapy be offered, and what is it?
Offer after 8 weeks of no improvement.
**Vitamin D analogue** applied BD (increased from OD)
48
What are the third-line topical options if psoriasis remains unresponsive after 8–12 weeks?
Potent corticosteroid twice daily for up to 4 weeks.
Coal tar preparation once or twice daily.
Short-acting dithranol.
49
What are the primary phototherapy options in secondary-care management of psoriasis?
* **Narrowband ultraviolet B (NB-UVB)**: treatment of choice; ideally 3×/week.
* **PUVA (psoralen + UVA) photochemotherapy.**
50
What adverse effects are associated with ultraviolet phototherapy?
Skin ageing.
Increased risk of squamous cell carcinoma (not melanoma).
51
What are the systemic therapy options for moderate–severe plaque psoriasis?
* 1st: oral **methotrexate** (also for psoriatic arthritis).
* **Ciclosporin**.
* **Systemic retinoids**.
* **Biologics**: infliximab, etanercept, adalimumab.
* Emerging: **ustekinumab** (IL-12/IL-23 blocker).
52
How is scalp psoriasis managed according to NICE?
1. Potent topical corticosteroid once daily for 4 weeks.
2. If no improvement after 4 weeks: A) Change corticosteroid formulation (e.g. shampoo, mousse); B) salicylic aicd, emollients, oils
53
What is the management of face, flexural and genital psoriasis?
Mild–moderate potency corticosteroid applied once or twice daily, for a maximum of 2 weeks.
54
What precautions apply to topical corticosteroid use in psoriasis?
* Risk of skin atrophy, striae, rebound.
* Scalp, face, flexures prone to atrophy: limit to 1–2 weeks per month.
* Systemic effects if used on > 10 % body surface area.
* Aim for 4-week break before a new course.
* Potent steroids: maximum 8 weeks continuously; very potent: maximum 4 weeks continuously.
55
What are the key features of vitamin D analogues in psoriasis?
Examples: calcipotriol, calcitriol, tacalcitol.
Mode of action: ↓ keratinocyte division/differentiation → ↓ epidermal proliferation.
Reduce scale and plaque thickness (less effect on erythema).
Adverse effects uncommon; no smell or staining.
Suitable for long-term use (avoid in pregnancy).
Maximum adult dose: 100 g/week.
56
What is the mechanism and adverse effects of dithranol
Dithranol
* Inhibits DNA synthesis
* Apply for 30 minutes then wash off.
* AEs: local burning; skin staining.
57
What is the mechanism of adverse effects of coal tar
* Likely inhibits DNA synthesis.
* AEs: odour; staining.
58
What are the exacerbating factors of psoriasis?
* Trauma
* Alcohol
Drugs: **NABILA**
* **N**SAIDS
* **A**nti-malaris (chloroquine), **A**lcohol
* **B**eta blockers
* **I**nfliximab, **I**nterferon
* **L**ithium
* **A**CE inhibitors
59
Which demographic is most commonly affected by guttate psoriasis, and what precipitant is often implicated?
More common in children and adolescents.
Often precipitated by streptococcal infection 2–4 weeks before lesion onset.
60
Describe the characteristic clinical features of guttate psoriasis.
* ‘Tear-drop’ papules on trunk and limbs (“gutta” = drop).
* Pink, scaly patches or plaques.
* Acute onset over days.
61
What is the typical natural history of guttate psoriasis?
Most cases resolve spontaneously within 2–3 months.
62
What is the role of antibiotics in the management of guttate psoriasis?
No firm evidence supports antibiotics to eradicate streptococcal infection for psoriasis improvement.
63
What topical and phototherapy treatments are used for guttate psoriasis?
* Topical agents as per chronic plaque psoriasis (e.g. potent corticosteroids, vitamin D analogues).
* Ultraviolet B (UVB) phototherapy.
64
When might tonsillectomy be considered in guttate psoriasis?
In cases of recurrent episodes associated with streptococcal infection.
65
What prodromal history differentiates guttate psoriasis from pityriasis rosea?
**Guttate psoriasis**
* Clasically preceded by **streptococcal sore throat** 2-4 weeks before lesions
**Pityriasis rosea**
* May report recent URTI, but not common in questions
66
How do lesions of guttate psoriasis differ in appearance from those of pityriasis rosea
**Guttate psoriasis**
* 'Tear-drop' scaly papules on trunk and limbs
**Pityriasis rosea**
* Initial herald patch, then 1-2 weeks later multiple over erythematous, slightly raised lesions
* Fine scale at the periphery of lesions
* Often distributed along Langer's lines, producing a 'fir-tree' pattern
67
What are the differences in treatment and natural history between guttate psoriasis and pityriasis rosea?
**Guttate psoriasis:**
* Often resolves spontaneously within 2–3 months
* Topical psoriasis therapies (potent corticosteroids, vitamin D analogues)
* UVB phototherapy
* Consider tonsillectomy for recurrences
**Pityriasis rosea:**
* Self-limiting, resolves in around 6 weeks
* Symptomatic management (e.g. emollients, antihistamines)
68
What is bullous pemphigoid and what antigens are targeted?
Bullous pemphigoid is an autoimmune sub-epidermal blistering disorder in which circulating IgG autoantibodies target hemidesmosomal proteins BP180 (type XVII collagen) and BP230, leading to complement activation and dermo-epidermal separation.
## Footnote
None
69
Which patient population is most commonly affected by bullous pemphigoid?
Elderly individuals.
## Footnote
None
70
What are the hallmark cutaneous features of bullous pemphigoid?
Intensely pruritic, tense blisters arising on erythematous or urticated bases, often localized to flexural areas. Blisters typically heal without scarring.
## Footnote
None
71
How is bullous pemphigoid diagnosed histologically?
Sub-epidermal blister with an inflammatory infiltrate rich in eosinophils.
## Footnote
None
72
What does direct immunofluorescence reveal in bullous pemphigoid?
**Linear deposition of IgG** and **C3** at the **dermo-epidermal junction**.
## Footnote
None
73
What are the mainstays of management for bullous pemphigoid?
* Systemic corticosteroids: First-line therapy to control disease activity.
* Topical high-potency corticosteroids: Particularly in limited disease.
* Steroid-sparing agents: Azathioprine, methotrexate or mycophenolate mofetil for long-term control.
* Antibiotics with anti-inflammatory properties: Doxycycline or dapsone as adjunctive therapy.
## Footnote
None
74
What is cutaneous squamous cell carcinoma and how often does it metastasise?
Cutaneous squamous cell carcinoma is a malignant proliferation of epidermal keratinocytes. Metastatic spread is uncommon, occurring in approximately 2–5 % of cases.
## Footnote
None
75
What are the principal risk factors for squamous cell carcinoma of the skin?
* Chronic ultraviolet radiation (sunlight, PUVA therapy)
* Pre-malignant lesions: actinic keratoses, Bowen’s disease
* Immunosuppression (e.g. post-transplant, HIV)
* Smoking
* Chronic wounds (Marjolin’s ulcer)
* Genetic disorders (xeroderma pigmentosum, oculocutaneous albinism)
## Footnote
None
76
On which sites does squamous cell carcinoma typically arise and what are its clinical features?
* Predilection for sun-exposed areas (head, neck, dorsum of hands and arms)
* Presents as a rapidly enlarging, painless nodule that may ulcerate
* Surface can be hyperkeratotic or “cauliflower-like,” often with areas of bleeding
## Footnote
None
77
What are the mainstays of diagnosis and treatment for cutaneous squamous cell carcinoma?
* Diagnosis: Excisional or incisional skin biopsy demonstrating invasive atypical squamous cells forming keratin pearls.
* Treatment:
* Surgical excision with appropriate margins (typically 4–6 mm)
* Mohs micrographic surgery for high-risk or cosmetically sensitive sites
* Radiotherapy for inoperable lesions or adjuvant therapy in cases with perineural invasion
## Footnote
None
78
What are the recommended surgical excision margins for cutaneous squamous cell carcinoma based on lesion size?
* Lesions <20 mm diameter: 4 mm clinical margins
* Lesions ≥20 mm diameter: 6 mm clinical margins
## Footnote
None
79
When is Mohs micrographic surgery indicated for cutaneous squamous cell carcinoma?
Mohs surgery is reserved for patients at high risk of recurrence or metastasis and for tumours located in anatomically or cosmetically sensitive areas (e.g. periorbital region, lips, ears).
## Footnote
None
80
Which histological and clinical features predict a favourable prognosis in cutaneous squamous cell carcinoma?
* Well-differentiated tumour histology
* Maximum diameter <20 mm
* Invasion depth <2 mm
* Absence of immunosuppression
## Footnote
None
81
What features are associated with a poorer prognosis in cutaneous squamous cell carcinoma?
* Poorly differentiated tumour histology
* Maximum diameter >20 mm
* Invasion depth >4 mm
* Presence of any cause of immunosuppression (e.g. post-transplant, HIV)
## Footnote
None
82
What are the clinical features and common aetiologies of erythema nodosum?
Features: Symmetrical, tender, erythematous subcutaneous nodules on the shins that resolve without scarring.
Common causes: *Streptococcal infection* *sarcoidosis* *inflammatory bowel disease* *drug reactions (penicillins, sulphonamides, oral contraceptive pill).*
83
How does pretibial myxoedema present and with which endocrine disorder is it associated?
Presentation: Symmetrical, indurated, erythematous plaques on the anterior shins with a “peau d’orange” (orange-peel) texture.
Association: Graves’ disease (autoimmune hyperthyroidism).
84
What are the characteristic progression and associations of pyoderma gangrenosum?
Evolution: Begins as a small, erythematous papule or pustule, progressing to painful, deep ulceration with a violaceous, undermined border.
Associations: Idiopathic in ~50% of cases; also linked to *inflammatory bowel disease* *connective-tissue diseases* *myeloproliferative disorders.*
85
Describe the appearance and typical patient population for **necrobiosis lipoidica diabeticorum.**
Appearance: Well-demarcated, shiny, yellow-brown plaques on the shins, often with overlying telangiectasia.
Patient population: Most commonly observed in individuals with diabetes mellitus.
