Fiche de révision : Dermatitis and Psoriasis: Skin Inflammatory Disorders

📋 Course Outline

1. Pruritus Causes
2. Eczema Types
3. Atopic Dermatitis
4. Contact Dermatitis
5. Seborrheic Dermatitis
6. Psoriasis Pathogenesis
7. Psoriasis Subtypes
8. Pityriasis Rosea
9. Lichen Planus

📖 1. Pruritus Causes

🔑 Key Concepts & Definitions

• Pruritus: An unpleasant sensation that provokes the desire to scratch, often associated with skin or systemic conditions.
• Xerosis (Dryness): The most common cause of pruritus, characterized by dry, rough, and scaly skin, leading to itchiness.
• Primary Skin Diseases: Skin conditions directly causing pruritus, including inflammatory, infectious, or infestational dermatoses such as eczema, psoriasis, or scabies.
• Systemic Causes: Underlying internal diseases that manifest with pruritus, including liver, kidney, thyroid diseases, infections, malignancies, and neuropsychiatric disorders.
• Eczema (Dermatitis): An inflammatory skin disease marked by pruritus, redness, and skin changes, classified as acute or chronic.
• Contact Dermatitis: Skin inflammation resulting from contact with external irritants or allergens, presenting as eczematous plaques or vesicles.

📝 Essential Points

• Dry Skin (Xerosis) is the most prevalent cause of pruritus, especially in older adults and dry climates.
• Inflammatory skin diseases like eczema and psoriasis are common causes, often presenting with characteristic lesions and intense itching.
• Systemic illnesses such as liver or renal failure can cause generalized pruritus without primary skin lesions.
• Eczema (Dermatitis) can be atopic, contact, seborrheic, or other types, with atopic dermatitis being the most common, especially in children.
• Triggers for eczema exacerbation include irritants, allergens, sweating, harsh soaps, emotional stress, and bacterial infections.
• Complications include secondary infections (bacterial, viral), pigmentary changes, and ocular issues.
• Management involves identifying and avoiding triggers, moisturizing, topical anti-inflammatories, phototherapy, systemic medications, and adjunct therapies like antihistamines.
• Contact dermatitis diagnosis is confirmed via patch testing to identify specific allergens, with treatment focusing on allergen avoidance and topical steroids.

💡 Key Takeaway

Pruritus results from a complex interplay of skin and systemic factors; effective management hinges on accurate diagnosis, trigger avoidance, and appropriate topical or systemic therapy.

📖 2. Eczema Types

🔑 Key Concepts & Definitions

• Eczema (Dermatitis): A group of inflammatory skin diseases characterized by itchy, red, and rough papules or plaques, often with secondary changes such as scaling or lichenification.
• Pruritus: An intense itching sensation that prompts scratching, commonly associated with eczema.
• Acute Eczema: Rapid onset, presenting with edematous, erythematous papules and plaques, vesicles, oozing, and crusting.
• Chronic Eczema: Long-standing, with thickened plaques, scales, and lichenification due to repeated scratching and inflammation.
• Atopic Dermatitis: The most common type, often hereditary, with a tendency for allergic reactions, starting in infancy and improving with age.
• Contact Dermatitis: Skin inflammation caused by external contact with irritants or allergens, presenting as well-defined eczematous plaques.

📝 Essential Points

• Types of Eczema: Includes atopic, contact, seborrheic, asteatotic, stasis, nummular, disseminated, infective, and diaper dermatitis.
• Atopic Dermatitis: Usually begins in infancy, with flexural involvement in older children and adults; associated with other atopic conditions like asthma and allergic rhinitis.
• Triggers & Exacerbants: Irritants (harsh soaps, wool), allergens (dust mites, pollen), sweating, emotional stress, bacterial infections.
• Complications: Pigmentary changes, bacterial (impetiginization), viral (HSV, molluscum), and ocular issues.
• Management: Emphasizes trigger avoidance, daily moisturization, topical anti-inflammatories (steroids, calcineurin inhibitors), phototherapy, and systemic medications for severe cases.
• Contact Dermatitis: Diagnosed via patch testing; management involves identifying and avoiding allergens, and topical steroids.
• Seborrheic Dermatitis: Often yeast-related, affecting scalp and face; treated with antifungals and mild steroids.
• Chronicity & Relapses: Eczema tends to be relapsing; long-term management focuses on skin barrier repair and trigger control.

💡 Key Takeaway

Eczema encompasses various inflammatory skin conditions with common features of pruritus and relapsing inflammation, requiring tailored management strategies based on type, triggers, and severity.

📖 3. Atopic Dermatitis

🔑 Key Concepts & Definitions

• Atopic Dermatitis (AD): A common, chronic inflammatory skin disease characterized by itchy, red, and dry skin, often with relapsing episodes. It is part of the atopic triad, frequently associated with asthma and allergic rhinitis.

• Pruritus: An intense itching sensation that drives the urge to scratch, a hallmark symptom of AD.

• Xerosis: Dry skin, which is a primary feature of AD, resulting from impaired skin barrier function.

• Lichenification: Thickened, leathery skin with accentuated skin lines, often seen in chronic AD due to repeated scratching.

• Flexural Eczema: Typical distribution of chronic AD lesions on flexor surfaces such as the elbows and knees in older children and adults.

• Eczematous Lesions: Red, itchy papules, plaques, and sometimes vesicles or oozing, characteristic of AD.

📝 Essential Points

• Epidemiology: Affects 10-30% of children and 2-10% of adults; usually begins in infancy or childhood and improves with age.

• Pathogenesis: Multifactorial involving genetic predisposition (e.g., filaggrin mutations affecting skin barrier), environmental triggers, immune dysregulation (Th2 dominance), and skin barrier impairment.

• Associated Conditions: Frequently coexists with other atopic diseases such as asthma, allergic rhinitis, and food allergies.

• Clinical Features:

  • Infants: Eczematous lesions on cheeks, scalp, and extensor surfaces.
  • Older children/adults: Chronic eczema on flexors, with xerosis, pruritus, and lichenification.
  • Other signs: Periorbital darkening, Dennie-Morgan lines, hyperlinear palms, keratosis pilaris, and pityriasis alba.

• Triggers & Exacerbating Factors: Irritants (harsh soaps, wool), allergens (dust mites, pollen), sweating, emotional stress, bacterial infections (Staph), smoking.

• Complications: Pigmentary changes, bacterial (impetiginization), viral infections (HSV, molluscum), ocular issues.

• Management:

  • Proactive skin care: Daily moisturizing, trigger avoidance.
  • Topical treatments: Corticosteroids (potency based on severity), calcineurin inhibitors (Tacrolimus, Pimecrolimus), crisaborole.
  • Phototherapy: UVA/UVB.
  • Systemic medications: Cyclosporine, methotrexate, biologics (Dupilumab), in severe cases.
  • Adjuncts: Antihistamines, antimicrobial agents, bleach baths.

💡 Key Takeaway

Atopic dermatitis is a chronic, relapsing inflammatory skin disorder driven by genetic and environmental factors, characterized by pruritus, xerosis, and eczematous lesions, requiring a comprehensive approach including skin barrier repair and targeted anti-inflammatory therapies.

📖 4. Contact Dermatitis

🔑 Key Concepts & Definitions

• Contact Dermatitis: An inflammatory skin reaction caused by direct contact with an external agent, presenting as eczema, urticaria, or pigmentation changes.
• Irritant Contact Dermatitis: A non-immunologic, toxic skin reaction resulting from direct damage by irritants like soaps, acids, or alkalis; affects anyone exposed.
• Allergic Contact Dermatitis: A delayed hypersensitivity immune response to an allergen previously sensitized; involves T-cell mediated immune mechanisms.
• Patch Test: A diagnostic tool where suspected allergens are applied to the skin (usually back) to identify specific sensitivities; readings at 48 and 72 hours.
• Eczematous Plaque: Well-defined, scaly, inflamed skin lesion characteristic of contact dermatitis.
• Trigger Factors: External agents such as chemicals, plants, jewelry, or topical medications that provoke contact dermatitis.

📝 Essential Points

• Contact dermatitis accounts for a significant portion of skin reactions, with 80% irritant and 20% allergic types.
• Clinical presentation varies but typically involves well-demarcated eczematous plaques with possible vesicles or scales.
• Common irritants include soaps, solvents, acids, and alkalis; allergens include nickel, fragrances, preservatives, and plants.
• Diagnosis relies on history, clinical examination, and patch testing for allergic cases.
• Management involves identifying and avoiding triggers, topical corticosteroids, and patient education.
• Chronic or repeated exposure can lead to persistent dermatitis, pigmentation changes, or secondary infections.

💡 Key Takeaway

Contact dermatitis is a common inflammatory skin reaction caused by irritants or allergens, with diagnosis primarily through patch testing and management focusing on trigger avoidance and topical anti-inflammatory therapy.

📖 5. Seborrheic Dermatitis

🔑 Key Concepts & Definitions

• Seborrheic Dermatitis: A common, chronic inflammatory skin condition characterized by greasy, scaly, erythematous patches primarily affecting sebaceous gland-rich areas such as the scalp, face, and chest.
• Malassezia furfur: A lipophilic yeast implicated in the pathogenesis of seborrheic dermatitis, believed to contribute to inflammation and scaling.
• Sebum Production: Excessive sebum secretion is associated with seborrheic dermatitis, providing a favorable environment for Malassezia growth.
• Dandruff: Mild form of seborrheic dermatitis limited to the scalp, presenting as flaky scalp scales without significant inflammation.
• Crusting and Scaling: The hallmark features include yellowish crusts and greasy scales on erythematous skin.
• Triggers: Factors such as stress, cold weather, oily skin, and immunosuppression can exacerbate seborrheic dermatitis.

📝 Essential Points

• Epidemiology: Affects approximately 5% of the population, more common in males and adults aged 20-50 years.
• Pathogenesis: Involves an interplay between Malassezia yeast, increased sebum, and host immune response, leading to inflammation.
• Common Sites: Scalp, eyebrows, nasolabial folds, ears, chest, and body folds.
• Clinical Features: Greasy, yellowish scales, erythema, and pruritus; may cause hair loss if scalp is involved.
• Diagnosis: Primarily clinical; no specific lab tests needed. Skin scrapings can reveal Malassezia.
• Complications: Secondary bacterial infections, especially in immunocompromised patients.
• Management:
  • Topical antifungals (ketoconazole, ciclopirox) to reduce yeast proliferation.
  • Topical corticosteroids for inflammation control.
  • Moisturizers to restore skin barrier.
  • Lifestyle modifications: Regular washing, avoiding harsh soaps, managing stress.
• Prognosis: Chronic relapsing condition requiring ongoing management.

💡 Key Takeaway

Seborrheic dermatitis is a chronic, relapsing inflammatory skin disorder driven by Malassezia yeast and excess sebum, primarily managed with antifungal and anti-inflammatory therapies to control symptoms and prevent flare-ups.

📖 6. Psoriasis Pathogenesis

🔑 Key Concepts & Definitions

• Epidermal Hyperproliferation: Accelerated growth and turnover of keratinocytes leading to thickened, scaly plaques due to increased DNA synthesis and cell division.

• Immune Dysregulation: Abnormal activation of innate and adaptive immune responses, particularly T cells, resulting in inflammation and keratinocyte proliferation.

• Genetic Factors: Hereditary predisposition involving multiple genes, notably HLA-CW6, which increases susceptibility to psoriasis.

• Trigger Factors: External or internal stimuli such as trauma (Koebner phenomenon), stress, infections, certain medications, and lifestyle factors that initiate or exacerbate psoriasis.

• Inflammatory Cytokines: Key signaling proteins like TNF-α, IL-17, IL-23, which mediate inflammation, keratinocyte activation, and sustain the psoriatic process.

• Koebner Phenomenon: The appearance of psoriatic lesions at sites of skin trauma or injury, indicating the role of skin injury in disease activation.

📝 Essential Points

• Psoriasis involves a multifactorial pathogenesis with genetic predisposition and environmental triggers.

• The immune system plays a central role, with T cell activation leading to cytokine release that promotes keratinocyte hyperproliferation.

• Keratinocyte abnormalities result in rapid cell turnover, abnormal differentiation, and the formation of characteristic plaques with silvery scales.

• The genetic component is polygenic, with HLA-CW6 being a significant genetic marker.

• Trigger factors such as trauma, stress, infections, and certain drugs can initiate or worsen the disease via immune activation.

• The Koebner phenomenon exemplifies how skin injury can induce new psoriatic lesions.

💡 Key Takeaway

Psoriasis is a complex immune-mediated disorder driven by genetic susceptibility and environmental triggers that lead to immune dysregulation, keratinocyte hyperproliferation, and characteristic skin lesions.

📖 7. Psoriasis Subtypes

🔑 Key Concepts & Definitions

• Plaque Psoriasis: The most common subtype characterized by well-defined, erythematous plaques with silvery-white scales, often on elbows, knees, and scalp.
• Guttate Psoriasis: Presents as small, drop-shaped lesions, often following infections like streptococcal pharyngitis.
• Inverse Psoriasis: Affects skin folds (axillae, groin, intergluteal), with smooth, erythematous, and shiny plaques lacking scales.
• Pustular Psoriasis: Characterized by white pustules on erythematous skin; can be generalized, palmoplantar, or localized (e.g., acrodermatitis continua of Hallopeau).
• Erythrodermic Psoriasis: Severe, widespread redness covering most of the body surface, often with systemic symptoms; requires urgent management.
• Nail Psoriasis: Involves nail dystrophy, pitting, onycholysis, and subungual hyperkeratosis, often associated with psoriatic arthritis.

📝 Essential Points

• Pathogenesis: Multifactorial involving epidermal hyperproliferation, immune dysregulation (T cell activation), and genetic predisposition (notably HLA-CW6).
• Common Triggers: Trauma (Koebner phenomenon), stress, infections, certain medications, smoking, and alcohol.
• Distribution: Plaque psoriasis favors scalp, elbows, knees, lower back; inverse affects skin folds; guttate often follows infections.
• Associated Conditions: Psoriatic arthritis (30% of patients), metabolic syndrome, cardiovascular diseases.
• Treatment Approaches:
  • Mild to moderate: Topical corticosteroids, vitamin D analogs, calcineurin inhibitors.
  • Moderate to severe: Phototherapy, systemic agents (methotrexate, cyclosporine, retinoids), biologics (anti-TNF, IL inhibitors).
  • Pustular and erythrodermic forms often require systemic and urgent interventions.

💡 Key Takeaway

Psoriasis is a chronic, immune-mediated skin disease with diverse subtypes that vary in presentation and severity; understanding these differences guides targeted and effective treatment strategies.

📖 8. Pityriasis Rosea

🔑 Key Concepts & Definitions

• Pityriasis Rosea: An acute, self-limiting skin condition characterized by the sudden appearance of a herald patch followed by a generalized rash with collarette scales, often in a Christmas tree pattern on the trunk.
• Herald Patch: The initial, single, oval or round, erythematous lesion with fine scale, typically larger than subsequent lesions, appearing 1-2 weeks before the generalized rash.
• Etiology: Believed to be viral, possibly related to human herpesviruses HHV6 & HHV7, with infectious and immune components involved.
• Rash Characteristics: Multiple erythematous, oval patches or plaques with fine scales, often arranged in a Christmas tree pattern along skin cleavage lines.
• Prodrome: Pre-rash symptoms such as fever, sore throat, or gastrointestinal disturbances may precede the rash.
• Course & Duration: Usually lasts 6-8 weeks, resolves spontaneously without treatment, but symptomatic relief with antihistamines and topical steroids can be used for pruritus.

📝 Essential Points

• Epidemiology: Common in teenagers and young adults; no gender predilection.
• Pathogenesis: Likely immune-mediated, possibly triggered by viral infection.
• Diagnosis: Primarily clinical; characteristic herald patch and pattern of rash are diagnostic.
• Differential Diagnosis: Tinea corporis, secondary syphilis, drug eruptions, psoriasis.
• Management: Mainly supportive—antihistamines for itching, topical steroids; no specific antiviral treatment needed.
• Complications: Rare; may include persistent pruritus or secondary bacterial infection.
• Prognosis: Excellent; resolves spontaneously with no scarring.

💡 Key Takeaway

Pityriasis Rosea is a common, self-limited skin eruption with a characteristic herald patch and a Christmas tree pattern rash, primarily managed with symptomatic treatment due to its benign and transient nature.

📖 9. Lichen Planus

🔑 Key Concepts & Definitions

• Lichen Planus: An idiopathic, inflammatory, autoimmune disease affecting the skin and mucous membranes, characterized by polygonal, flat-topped, purple papules with pruritus.

• Wickham Striae: Fine, white, lace-like lines seen on the surface of lichen planus papules, especially on mucous membranes; a hallmark feature.

• Pathogenesis: Believed to be T cell-mediated autoimmune reaction targeting basal keratinocytes, possibly triggered by infections, medications, or vaccines.

• Common Sites: Skin (flexor surfaces of wrists, ankles), oral mucosa (buccal mucosa), genitalia, nails, and scalp.

• Clinical Variants:

  • Cutaneous: Polygonal, purple, flat-topped papules; pruritic.
  • Mucosal: Erosive or reticular (Wickham striae), often painful.
  • Nail: Ridging, thinning, or pterygium formation.
  • Scalp: Scarring alopecia.

📝 Essential Points

• Diagnosis: Based on clinical appearance, presence of Wickham striae, and histopathology showing band-like lymphocytic infiltrate at the dermoepidermal junction with hyperkeratosis and sawtooth rete ridges.

• Associations: Possible links with hepatitis C virus (HCV), medications, and vaccines; controversial but noteworthy.

• Management:

  • Topical corticosteroids: First-line for skin and mucous membrane lesions.
  • Topical calcineurin inhibitors: Tacrolimus, pimecrolimus for mucosal lesions.
  • Systemic therapy: Oral corticosteroids, retinoids, cyclosporin, methotrexate for severe or resistant cases.
  • Phototherapy: NB-UVB or PUVA for extensive skin involvement.
  • Monitoring: Risk of malignant transformation, especially in oral lesions.

• Prognosis: Usually chronic with remissions and exacerbations; mucosal erosive forms may be painful and persistent.

💡 Key Takeaway

Lichen planus is a T cell-mediated autoimmune disease presenting with characteristic purple, polygonal papules and Wickham striae, requiring a combination of clinical, histological, and sometimes laboratory assessments for diagnosis and management.

📊 Synthesis Tables

⚠️ Common Pitfalls & Confusions

1. Confusing xerosis with eczema as primary cause of pruritus; xerosis is a common trigger but not always the primary disease.
2. Mistaking allergic contact dermatitis for irritant contact dermatitis; history and patch testing differentiate.
3. Overlooking systemic causes of pruritus, especially in elderly patients with generalized itch without primary skin lesions.
4. Assuming all eczematous lesions are atopic dermatitis; contact dermatitis and other types can mimic it.
5. Using topical steroids indiscriminately without identifying triggers or underlying conditions.
6. Misidentifying seborrheic dermatitis as psoriasis or eczema; location and response to antifungals help differentiate.
7. Ignoring the significance of skin barrier defects in atopic dermatitis and their role in disease management.
8. Confusing psoriasis subtypes; plaque psoriasis is most common, but pustular, guttate, and inverse forms exist.
9. Misdiagnosing pityriasis rosea as psoriasis or eczema; herald patch and distribution are clues.
10. Overlooking the characteristic violaceous, polygonal, flat-topped lesions of lichen planus.

✅ Exam Checklist

• Identify common causes of pruritus, including xerosis, systemic diseases, and primary skin conditions.
• Differentiate between types of eczema: atopic, contact, seborrheic, stasis, nummular.
• Describe the pathogenesis, clinical features, and management of atopic dermatitis.
• Recognize clinical features and triggers of contact dermatitis; explain the role of patch testing.
• Compare seborrheic dermatitis with other eczematous conditions regarding location and etiology.
• Outline the pathogenesis, clinical presentation, and treatment options for psoriasis, including subtypes.
• Describe the typical presentation and distribution of pityriasis rosea.
• Recognize the characteristic lesions, distribution, and histology of lichen planus.
• Understand the importance of skin barrier function in eczema and atopic dermatitis.
• List systemic causes of generalized pruritus.
• Know the main therapeutic strategies for inflammatory and allergic skin conditions.
• Differentiate between acute and chronic eczema based on clinical features.