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Questions and Answers
What is a potential temporary adverse outcome following a treatment?
Which biopsy technique is best suited for cosmetically sensitive areas like the face?
What feature distinguishes excision biopsy from incision biopsy?
What is the complication related to wound design?
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Which technique is recommended for obtaining the best pathological specimen?
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What type of scarring is typically associated with punch biopsies?
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What is the purpose of having excision margins of 2mm to 5mm for benign lesions?
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Which of the following is a permanent adverse outcome of surgical treatment?
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Which of the following factors can exacerbate Atopic Dermatitis (AD)?
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What is the primary feature of the 'inside-out' hypothesis regarding Atopic Dermatitis?
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Which skin condition is characterized by spongiosis?
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What does an increase in IgE indicate in the context of Atopic Dermatitis?
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Which of the following skin microbiome changes is associated with Atopic Dermatitis?
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What is commonly observed in chronic Atopic Dermatitis?
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Which symptom is specifically related to severe pruritis in Atopic Dermatitis?
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What anatomical feature is primarily affected during the acute phase of Atopic Dermatitis?
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What is the primary advantage of using skin flaps over skin grafts?
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Which of the following suture materials is considered non-synthetic and absorbable?
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What is a critical pre-requisite for primary surgical wound repair?
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Which of the following describes the type of dermatitis caused by prolonged contact with an allergen?
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What mechanism primarily leads to the symptoms of acute dermatitis upon re-exposure to an allergen?
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In which scenario is delayed primary repair indicated?
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Which of the following components is typically seen in chronic eczema?
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What is the primary function of the epidermal protein 'Filaggrin' in the context of dermatitis?
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Which type of skin graft involves the removal of the entire dermis and epidermis from the original site?
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What is the typical time recommended for suture removal after surgical wound repair?
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What association is noted in the aetiology of seborrheic dermatitis?
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A common feature of stasis dermatitis is:
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Which population is most likely to develop stasis dermatitis?
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Which of the following is NOT a risk factor for seborrheic dermatitis?
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What primary clinical feature characterizes infantile seborrheic dermatitis?
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What treatment is appropriate for reducing dependent oedema in stasis dermatitis?
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Lichen simplex chronicus is primarily caused by:
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Which management option is used for treating the oozing patches in stasis dermatitis?
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What is a characteristic clinical manifestation of adult seborrheic dermatitis?
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What is one of the common complications associated with stasis dermatitis?
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Which condition is primarily associated with chronic itching due to hyperkeratosis and inflammation?
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What is the most common infectious trigger for erythema multiforme?
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Which feature is NOT typical of chronic lichenified eczema?
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What type of management is recommended for resolving plaques in chronic eczema?
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During which ages is erythema multiforme most commonly observed?
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Which of the following is NOT a feature of erythema multiforme morphology?
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Which of the following is often a psychosomatic cause associated with chronic itching?
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What is a typical initial treatment option for a patient presenting with a chronic dermatitis flare-up?
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Study Notes
Expected Adverse Outcomes
- Pain can be expected during and after the treatment.
- Oedema and swelling may occur at the treated site and surrounding tissues.
- Vesicle and bulla formation is another possible outcome.
- Exudation weeping and crust formation are also expected outcomes.
Temporary Adverse Outcomes
- Hypopigmentation is possible, but usually temporary.
- Hyperpigmentation can also occur, but is often temporary.
- Secondary infection may occur, which can be managed with antibiotics.
Permanent Adverse Outcomes
- Permanent Hypopigmentation is possible, and can be a significant concern for patients.
- Scarring + Possible Retraction can occur, especially with more severe skin lesions.
- Allopecia (hair loss) is another potential permanent adverse outcome.
- Nail Dystrophy is a possible complication of certain procedures.
Biopsy Techniques
- Many biopsy techniques exist, each suited to different lesion types and information needs.
- Punch biopsy leaves minimal scarring and is ideal for cosmetically sensitive areas like the face.
- Shave biopsy is a quick and easy technique for nodular, easily removable lesions.
- Curette biopsy is similar to the shave biopsy, also quick and easy with minimal equipment.
- Incision biopsy offers the best specimen for pathologic assessment, requiring a biopsy set and sutures.
- Excision biopsy involves excising the entire lesion, providing a good pathology specimen.
Wound Design
- Relaxed skin tension lines (RSTL) and cosmetic junction lines (CJL) should guide wound design to minimize scarring.
- Excision margins vary depending on the lesion type, with 2mm to 5mm for benign and wider for malignant lesions.
Surgical Wound Repair
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Suture materials are categorized into:
- Synthetic Non-Absorbable: Nylon and Polypropylene, used on external surfaces for easy removal.
- Synthetic Absorbable: Monocryl and Vicryl (Polylactin), broken down by the body.
- Non-Synthetic Non-Absorbable: Silk.
- Non-Synthetic Absorbable: Catgut (being phased out).
- Suture sizes range from 1 to 6, with 1 being the thinnest and 6 the thickest.
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Surgical wound repair types include:
- Primary Repair: Performed within 6-8 hours.
- Delayed Primary Repair: Performed within 72 hours, often for surgical conditions.
- Secondary Repair: Performed after 72 hours, also used for surgical conditions.
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Pre-requisites for surgical wound repair:
- A clean wound: eliminate dead tissue, dead space, hematoma, and foreign bodies.
- Finest suture material: minimize tension and risk of scarring.
- Suture removal at appropriate time: Varies depending on the site of injury.
Skin Grafts Vs Skin Flaps
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Skin grafts are detached tissue with no intrinsic blood supply, requiring grafting onto vascularized tissue.
- Full Thickness Graft (FTG) includes all dermis and epidermis.
- Split Skin Graft (SSG) includes epidermis with some superficial dermis.
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Skin flaps remain connected to their original location with intrinsic blood supply.
- Indications for skin flaps: Poor vascularity, vital structures, and cosmetic concerns.
- Types of Skin Flaps: Rotation, advancement, and transposition.
- "Free" Flaps are skin grafts where blood supply is restored via microsurgery.
Dermatitis (Eczema)
Acute Dermatitis/Eczema
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Types of Acute Eczema:
- Contact Dermatitis: due to prolonged exposure to allergen.
- Atopic Dermatitis: subtypes include drug eczema, photoeczema, and primary irritant dermatitis.
- Aetiology: Prolonged contact with allergens like urine, soaps, etc.
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Epidemiology:
- strong family history in 70% of cases.
- Most common in children.
- Genetic component with 50% of patients deficient in filaggrin.
- Hypersensitivity often linked to other atopic conditions like hay fever and asthma.
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Pathogenesis:
- Initial exposure: allergen processing by Langerhans cells, T-cell activation in lymph nodes.
- Re-exposure: Type IV hypersensitivity (T-cell mediated) reaction, epidermal oedema and small blisters (wet eczema).
- Chronic exposure: hyperplasia, hyperkeratosis (lichenification) (dry eczema).
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Morphology:
- Gross: erythema, small blisters, hyperkeratosis (chronic).
- Microscopic: epidermal blistering, intra-epidermal oedema (spongiosis), perivascular inflammatory infiltrate.
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Clinical Features:
- Severe itching.
- Patchy, erythematous, poorly defined rash.
- Common locations: popliteal/cubital fossae and face; can be generalised.
- Dry Skin: excoriation, lichenification, crusting, weeping.
- Contact Dermatitis: often has a regular shape (e.g., square from Band-Aid).
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Treatment:
- Modify lifestyle: avoid exacerbating factors.
- Remove allergen.
- Avoid soaps.
- Use moisturisers and bath additives.
- Topical corticosteroids: for symptomatic relief.
- Antihistamines: for itching.
Atopic Dermatitis: Pathogenesis and clinical findings
| Category | Description |
|---|---|
| Impaired Epidermal Barrier | (e.g.fillagrin and SPINK5 gene mutations) |
| Increased trans-epidermal water loss | Exacerbation by long hot showers, sweating, stress |
| Xerosis | Note: It is not yet fully understood if Atopic Dermatitis (AD) is initiated by skin barrier dysfunction ("outside-in" hypothesis), or immune dysregulation ("inside-out" hypothesis) |
| Innate Immune System Defects | Defects in cell-mediated epidermal barrier repair process result in inflammation and leaky junctions between cells |
| Impaired Epidermal Barrier | Disruption of stratum corneum allows penetration of irritants, microbes & antigens.Exacerbation by irritants and allergens: detergents, solvents, hard water, clothing, environmental aero-allergens (e.g.dust mites) |
| Stimulation of cutaneous itch receptors | Pruritis |
| Skin Infection | ↑ susceptibility to pathogenic cutaneous infections |
| Adaptive Immune System Defects | Overexpression of Type 2 helper (Th2) cytokines and IgE in response to antigens.AD is commonly seen in people with a family history of atopic disease eg.allergic rhinitis, food allergy, asthma |
| Altered Skin Microbiome | Skin colonization e.g.S.aureus may be an AD trigger (via toxin release) or a consequence |
| Immune Dysregulation: Acute | Keratinocyte release of cytokine mediators - ↑Th2 & ↑ IgE |
| Intracellular edema within epidermal layer, resulting in intraepidermal vesicles | Spongiosis |
| ↑ IgE | |
| Immune Dysregulation: Chronic | Chronic disease punctuated by acute flares with slow resolution.Hyperplasia of keratinocytes within stratum corneum (uppermost layer), resulting in excessive accumulation of fibrous protein keratin. |
| Hyperkeratosis | Scale |
| Acute: Inflammation of dermis | Acute AD |
| Chronic: Hyperplasia of subcorneal epidermis (second layer) causes skin thickening and accentuated skin markings | Chronic AD |
| Disruption of vesicles from scratching | Severe Pruritis |
| Erythema | |
| Lichenification | Plaques |
| Spongiosis | |
| Oozing | |
| Crusting | |
| Dry Scale | |
| Dermal-Epidermal Junction | |
| Dermal layer | |
| Lichenification | Severe Pruritis |
| Hyperkeratosis |
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Distribution:
- Infants (<6 months): face, scalp, extensor surface of elbow.Primarily vesiculopapules.- Children (> 18 months - puberty): neck, extensor surface of elbows and knees.Primarily juicy papules.- Adults (beyond puberty): Forehead, neck, hands, feet.Primarily thick, dry, lichenified plaques.- Legend:
- Pathophysiology
- Mechanism
- Sign/Symptom/Lab Finding
- Complications
Seborrheic Dermatitis
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Aetiology:
- Possible hereditary component.
- Association with Malassezia yeast, with inflammatory reactions potentially caused by fatty acid metabolites.
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Risk Factors:
- Oily skin.
- Familial history of dermatitis/psoriasis.
- Immunosuppression.
- Parkinson's disease.
- Sleep deprivation and stress.
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Epidemiology:
- Bimodal onset: infancy (within the first months) or between 20-50 years old.
- More common in males.
- Pathophysiology: Not completely understood.
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Clinical Features:
- Chronic/relapsing eczema, tending to improve in summer and worsen in winter.
- Primarily affects sebaceous-rich areas like the scalp, face, and trunk.
- Ill-defined, localized scaly patches/scale.
- Blepharitis (scaly red eyelid margins).
- Salmon-pink thin scaly and ill-defined plaques in skin folds.
- Infantile Seborrheic Dermatitis: numerous dermatoses in the first 3 months of life, erythematous but non-itchy rash involving the face, scalp, neck, axillae, and nappy area.
- Adult Seborrheic Dermatitis: erythema and fine, greasy scale on the cheeks, nose, and nasolabial folds; scale and itching of the scalp and eyebrows; well-defined but non-scaly erythema of the axillae, groin, scrotum, and perianal skin.
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Management:
- Keratolytics (e.g., Salicylic Acid).
- Topical antifungals (e.g., Ketoconazole).
- Mild topical steroids.
- Isotretinoin for moderate/severe seborrheic dermatitis.
Stasis Dermatitis (Venous Eczema)
- Aetiology: Venous insufficiency combined with gravity.
- Epidemiology: Middle-aged to older patients, affecting about 20% of individuals over 70 years old.
- Risk factors: History of DVT in the affected limb, varicose veins, venous leg ulcers.
- Pathophysiology: Venous insufficiency leading to failure of the calf pump mechanism, causing blood pooling, increased venous hydrostatic pressure, and oedema. The fluid accumulation activates the innate immune response.
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Clinical Features:
- May form distinct patches or become confluent/circumferential.
- Itchy red, blistered, and crusted plaques on one or both lower legs.
- Orange-brown macular pigmentation due to haemosiderin deposition.
- Champagne bottle shape of the lower leg.
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Management:
- Reduce Dependent Oedema: elevate feet when sitting, walk regularly, elevate feet overnight, wear graduated compression stockings long-term.
- Treat Eczema: dry up oozing patches with potassium permanganate or dilute vinegar, oral antibiotics for infection prevention, topical steroids, moisturising cream, avoid skin injury.
- Treat Varicose Veins: consult a vascular surgeon, consider sclerotherapy or laser treatment.
Lichen Simplex Chronicus
- Aetiology: Repetitive scratching and rubbing due to chronic localized itch caused by conditions like atopic eczema, contact eczema, venous eczema, psoriasis, lichen planus, or fungal infection.
- Epidemiology: Affects both males and females, uncommon in children, associated with anxiety and/or obsessive-compulsive disorder (OCD).
- Pathophysiology: Repetitive scratching/rubbing leads to hyperkeratosis and inflammation.
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Clinical Features:
- Chronic, lichenified eczema/dermatitis.
- Single or multiple plaques.
- Dry, scaly surface.
- Leathery induration.
- Scratch marks.
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Management:
- Potent topical steroids for 4-6 weeks until the plaque resolves.
- Coal tar preparations.
- Moisturisers.
- Antihistamines for itch.
- Antidepressants for psychosomatic causes.
Erythema Multiforme:
- Aetiology: Hypersensitivity reaction, some genetic predisposition with HLA-B15, -B35, A33, -DR53, -DQB1*0301.
- Pathogenesis: Hypersensitivity response to infections (Herpes simplex, Mycoplasma), drugs (sulphonamides, penicillin, barbiturates), malignancy (carcinoma, lymphoma), autoimmune conditions (e.g., lupus, SS, dermatomyositis).
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Morphology:
- Gross: variable lesions (papules, plaques, nodules, blisters, ulcers) with characteristic "targetoid" lesions (central grey necrosis and erythematous raised border).
- Microscopic: dyskeratosis, necrotic keratinocytes, spongiosis (epidermal oedema), epidermal lymphocytes, destruction of the basal epidermal layer.
- Clinical Features: Acute and self-limiting, commonly affects young adults (20-40 years old).
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Description
This quiz focuses on the adverse outcomes associated with biopsy procedures, including expected, temporary, and permanent effects. It also delves into various biopsy techniques and their relevance to different skin lesions. Test your knowledge of the complications and management strategies during and after treatment.
