Lernzettel: 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

Feature	Atopic Dermatitis	Contact Dermatitis
Etiology	Genetic predisposition, immune dysregulation	External irritants or allergens
Pathogenesis	Skin barrier defect + Th2 immune response	T-cell mediated hypersensitivity (Type IV)
Typical Location	Flexural areas, face, hands	Site of contact with allergen/irritant
Onset	Usually in infancy or childhood	Any age, depends on exposure
Chronicity	Recurrent, relapsing	Usually resolves with allergen avoidance
Associated Conditions	Asthma, allergic rhinitis	Usually isolated, no systemic association
Key Features	Itching, xerosis, lichenification	Erythema, vesicles, edema, crusting

Treatment Approach	Atopic Dermatitis	Contact Dermatitis
Trigger avoidance	Yes	Yes
Moisturization	Essential	Essential
Topical steroids	Yes, potency based on severity	Yes, for inflammation
Calcineurin inhibitors	Yes (Tacrolimus, Pimecrolimus)	Yes (if allergic contact dermatitis)
Phototherapy	Yes	Rarely
Systemic therapy	Severe cases (biologics, immunosuppressants)	Not typical unless severe or widespread

⚠️ 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.