Common Papulosquamous Skin Disorders (INTEGUMENTARY SYSTEM) PDF

Y2B10M1L5 LECTURER: DR. HAIDER H. REYES, MD, MPH, DPDS INTEGUMENTARY SYSTEM OCTOBER 3, 2024 | 10:00-12:00 COM...

Y2B10M1L5 LECTURER: DR. HAIDER H. REYES, MD, MPH, DPDS INTEGUMENTARY SYSTEM OCTOBER 3, 2024 | 10:00-12:00 COMMON PAPULOSQUAMOUS SKIN DISORDERS TABLE OF CONTENTS I. Introduction G. Prognosis A. Papulosquamous V. Pityriasis Rubra Pilaris Reaction Pattern A. Clinical Case 4 II. Psoriasis B. Epidemiology A. Clinical Case 1 C. Types of PRP B. Epidemiology D. Etiology and C. Types of Psoriasis Pathogenesis D. Nail Changes in E. Diagnosis Figure 2. Layers of the skin Psoriasis F. Management E. Pathogenesis G. Prognosis II. PSORIASIS F. Risk Factors VI. Parapsoriasis A. CLINICAL CASE 1 G. Diagnosis A. Clinical Case 5 H. Treatment B. Large Plaque A 64-year-old female came in for consultation with a 2-month I. Prognosis Parapsoriasis history of the following lesions. III. Seborrheic Dermatitis C. Small Plaque A. Clinical Case 2 Parapsoriasis B. General Features D. Etiology and C. Clinical Presentation Pathogenesis D. Etiology and E. Management Pathogenesis F. Prognosis E. Management VII. Pityriasis Lichenoides F. Prognosis A. Clinical Case 6 Figure 3. Psoriasis IV. Pityriasis Rosea B. Epidemiology 1. What is the primary and secondary lesion? A. Clinical Case 3 C. Clinical Features ○ Primary: Plaques/Papules B. Epidemiology D. Complications ○ Secondary: Scales C. Clinical Features E. Etiology and 2. How would you describe the skin findings? D. Etiology and Pathogenesis ○ Multiple erythematous papules and scaly plaques over Pathogenesis F. Diagnosis the trunk and extremities. E. Diagnosis G. Management 3. What important physical findings do you need to check for this F. Management VIII. Exercises case? ○ Nails I. INTRODUCTION 4. What is the diagnosis? A. PAPULOSQUAMOUS REACTION PATTERN ○ Psoriasis Vulgaris Primary lesion - relatively thin or flat-topped papule or plaque Lecturer Notes: with scale Table 1. Lesions Crust or lichenification - may or may not be present TYPES OF LESIONS Flat Macule Patch (larger) PRIMARY Raised Papule LESIONS Patch (larger) Macule Vesicle Bulla (larger) SECONDARY Scaling LESIONS Fissure Describing lesions ○ Number: Multiple/solitary ○ Color → Hyperpigmented/hypopigmented Figure 1. Papulosquamous reaction pattern → Erythematous/yellowish Histopathologically, these processes involve the epidermis ○ Site and superficial to mid-dermis ○ Distribution: Generalized/localized 🔊🗃️ MG 2 | MG 9 1 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS KOEBNER PHENOMENON In dermatology, it is important to check not just the skin, but also the nails, hair, and intimate areas like the genitals. Isomorphic response ○ Sometimes, patients don’t disclose everything. Traumatic induction of psoriasis on nonlesional skin All-or-none phenomenon B. EPIDEMIOLOGY 7 to 14 days after injury 25-75% of patients may develop at some point during disease Worldwide occurrence Prevalence: 0.1%-3% Males = Females Age on onset: 15-30 years old Multifactorial inheritance: Polygenic + Environmental C. TYPES OF PSORIASIS PLAQUE TYPE Most common type Classic lesion: well-demarcated, raised, red plaques with white scaly “silvery” surface. Symmetric Figure 7. Koebner Phenomenon (A: Psoriasis appearing in keratome biopsy sites 4 weeks after biopsy; B: Flare of psoriasis Figure 4. Plaque Psoriasis on the back after sunburn. Note sparing of sun-protected areas.) Areas of lesions: ○ Extensor aspects of the extremities (elbows and knees) GUTTATE ○ Scalp Latin gutta = “a drop” ○ Lower lumbosacral Eruption of small papules (0.5-1.5 cm in diameter) ○ Buttocks Areas of Predilection: upper trunk and proximal extremities ○ Genital Area Early age ○ Umbilicus Associated with: ○ Intergluteal cleft ○ HLA-Cw6 (strongest) ○ Streptococcal throat infection Figure 8. Guttate Psoriasis Figure 5. Plaque Psoriasis SMALL PLAQUE AUSPITZ SIGN Resembles guttate psoriasis clinically Pinpoint bleeding at the top of ruptured capillaries with Onset in older patients forcible removal of outer scales from a psoriatic plaque. Chronic course Larger lesions (typically 1-2 cm) Thicker and scalier INVERSE Localized in the major skinfolds (i.e axillae, genitocrural region, and neck) Scaling is usually minimal or absent Glossy sharply demarcated erythema Figure 6. A. Auspitz Sign; B. Point of bleeding after scale removal Sweating is impaired in affected areas MG 2 | MG 9 2 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS A. GENERAL PUSTULAR PSORIASIS (VON ZUMBUSCH TYPE) Acute variant Usually preceded by other forms of the disease Fever + sudden generalized eruption of sterile pustules 2 to 3 mm in diameter Areas affected: Trunks and extremities, including nail beds, palms, and soles Figure 9. Inverse Psoriasis ERYTHRODERMIC Affects all body sites: face, hands, feet, nails, trunk, and extremities Erythema - most prominent feature Superficial scaling Risk of hypothermia ○ Lose excessive heat because of generalized vasodilation ○ Shiver in an attempt to raise their body temperature. Figure 12. General Pustular Psoriasis (von Zumbusch type) Provoking agents: ○ Infections ○ Irritating topical treatment (Koebner phenomenon) ○ Withdrawal of corticosteroids → Some patients seen by general practitioners thinking that it is just a rash and are given oral corticosteroids Few days after withdrawal, patient has psoriasis Complications: ○ Hypocalcemia ○ Bacterial superinfection ○ Sepsis – can lead to shock and death ○ Dehydration Figure 10. Erythrodermic Psoriasis PUSTULAR Clinical variants: a. Generalized Pustular Psoriasis (Von Zumbusch Type) b. Annular Pustular Psoriasis c. Impetigo Herpetiformis d. Pustulosis Palmaris et Plantaris e. Acrodermatitis Continua of Hallopeau Figure 13. von Zumbusch-type generalized pustular psoriasis. Figure 11. Pustular Psoriasis Note: tiny pustules, 1 to 2 mm in diameter, on erythematous skin. MG 2 | MG 9 3 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS B. ANNULAR PUSTULAR PSORIASIS Annular configuration of lesion Additional Information from Fitzpatrick: Annular Pustular Psoriasis ○ Usually presents in an annular or circinate form ○ Lesions may appear at onset of pustular psoriasis or develop during course of generalized pustular psoriasis ○ Lesions have a tendency to spread and form enlarged rings ○ Characteristic Features: pustules on a ring-like erythema Figure 16. Palmoplantar pustulosis Figure 17. Pustulosis Palmaris et Plantaris on hands & feet E. ACRODERMATITIS CONTINUA OF HALLOPEAU (DERMATITIS REPENS) Figure 14. Annular psoriasis on the flank (Fitzpatrick) Causes osteolysis ○ Melts bone due to ongoing inflammatory reaction C. IMPETIGO HERPETIFORMIS Onset: 3rd trimester of pregnancy (persists until delivery) Additional Information from Fitzpatrick: In most patients: Resolution after giving birth Acrodermatitis Continua of Hallopeau ○ Some may still develop clinically and progress into ○ Extremely rare psoriasis ○ Localized sterile pustular eruption of fingers and toes Often associated with hypocalcemia (from Fitzpatrick) ○ Typically involves distal portions of fingers and toes ○ May occur after minor trauma or infection ○ More common in middle-aged women Figure 15. Impetigo Herpetiformis Figure 18. Acrodermatitis continua of Hallopeau (Doc’s patient) D. PUSTULOSIS PALMARIS ET PLANTARIS Areas affected: Palms and soles Additional Information from Fitzpatrick: Pustulosis Palmaris et Plantaris ○ More common in females with median onset of 47 y.o. ○ Strongly associated with smoking ○ Difficult to treat, and often unresponsive to treatments used for chronic plaque psoriasis Figure 19. Acrodermatitis continua of Hallopeau MG 2 | MG 9 4 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS SEBOPSORIASIS Presents with erythematous plaques with greasy scales localized to seborrheic areas ○ Seborrheic Areas: scalp, glabella, nasolabial folds, perioral and pre-sternal areas, intertriginous area Relatively resistant to treatment ○ Antifungal Agents – may be useful Common Trigger: Stress Sebopsoriasis vs Seborrheic Dermatitis ○ Sebopsoriasis – lesion extending BEYOND hairline (either front or back) ○ Seborrheic Dermatitis - plaques ON SCALP ONLY Figure 23. Linear psoriasis (Doc’s patient) ○ In the absence of typical findings of psoriasis elsewhere, distinction from seborrheic dermatitis is difficult D. NAIL CHANGES IN PSORIASIS → Need to check for other findings (e.g. nails) 40% of patients Rare in absence of disease elsewhere Increases with age, duration, and extent of disease, and with presence of psoriatic arthritis Ask patient if they experience any joint pains, if nail findings of psoriasis are present NAIL PITTING One of the most common features of psoriasis Figure 20. Sebopsoriasis (Doc’s patient) Cause: defective keratinization Fingers > Toes Pits range from 0.5 to 2.0 mm in size Can be single or multiple ○ If >20 pits on the 10 digits = (+) psoriasis Figure 21. Sebopsoriasis NAPKIN PSORIASIS 3-6 months old (common in pediatric population) ○ Disappears after 1 y/o Course: Figure 24. Nail pitting (Fitzpatrick) ○ First appears in diaper/napkin area as confluent red OIL SPOTS patches ○ Few days later as small red papules on trunk Aka salmon spots or candle dripping → May also involve limbs Very specific nail finding for psoriasis → Face may be involved with red scaly eruption Characterized as translucent, yellow-red discolorations Responds readily to treatment observed beneath the nail plate often extending toward the hyponychium Causes: Psoriasiform hyperplasia ○ Parakeratosis ○ Microvascular changes ○ Trapping of neutrophils in nail bed Figure 22. Infant with napkin psoriasis LINEAR PSORIASIS Rare Linear lesions most common on limbs May also be limited to a dermatome on trunk May be an underlying nevus ○ Possibly an Inflammatory Linear Verrucous Epidermal Nevus (ILVEN) MG 2 | MG 9 5 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS PSORIATIC ARTHRITIS Seen in 40% of the patients Has a strong genetic component or predisposition Manifestations: ○ Peripheral arthritis ○ Spondyloarthritis ○ Enthesitis ○ Dactylitis Nail disease – known risk factor (80%) Figure 25. Top: Oil spots; Bottom: Distal onycholysis & oil drop NO topical treatment spotting ONYCHOLYSIS Separation of nail plate from nail bed ○ Lysis of nails (onycho-) Usually involves distal aspect of the nails Figure 26. Onycholysis ONYCHODYSTROPHY Nails are dystrophic Stronger association with psoriatic arthritis ○ Very debilitating Figure 28. Top: Psoriatic arthritis (Doc’s patient) KNOWN COMPLICATIONS OF PSORIATIC ARTHRITIS Increased morbidity & mortality from cardiovascular events Myocardial infarction – most common Metabolic syndrome (x 2.9) Rheumatoid arthritis Crohn’s disease and ulcerative colitis Hodgkin’s lymphoma Cutaneous T-cell lymphoma Figure 27.1. Onychodystrophy Depression and anxiety E. PATHOGENESIS Factors: ○ External environmental ○ Intrinsic genetic susceptibility ○ Cutaneous immune system plays a central role F. RISK FACTORS Obesity Heavy smoking (>20 cigarettes daily) ○ Also includes vaping Infections ○ i.e., Streptococcal throat, HIV, Hepatitis C infection Drugs ○ Antimalarials, β-blockers, lithium, nonsteroidal anti-inflammatory drugs (NSAIDs), IFNs-ɑ & γ, imiquimod, Figure 27.2. Onychodystrophy and loss of nails in a patient with angiotensin-converting enzyme inhibitors, and gemfibrozil psoriatic arthritis MG 2 | MG 9 6 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS G. DIAGNOSIS F. PROGNOSIS Clinical Diagnosis a. Guttate Psoriasis = self-limited ○ There are some cases that don’t fit the criteria for psoriasis b. Chronic Plaque Psoriasis = lifelong disease Histopathology ○ Once diagnosed with psoriasis, you live with it forever. ○ Done when we’re doubtful of our initial/working diagnosis c. Erythrodermic and Generalized Pustular Psoriasis ○ Sometimes, we tend to underestimate the cases, but when ○ Severe and persistent prognosis we examine via the microscope, it’s something different Younger age of onset and positive family history ○ More widespread and recurrent disease H. TREATMENT Variability in relapse Table 2. Psoriasis Treatment Frequently relapsing ○ Tend to have more severe disease with rapidly enlarging TREATMENT EXAMPLES lesions covering significant portions of the body surface Emollients ○ Rigorous treatment than those with more stable disease Steroids A history of onset of joint symptoms: 1st line Vitamin D3 Analogs ○ Before the 4th decade Topical Calcineurin Inhibitors ○ History of warm, swollen joints ○ Should raise the suspicion of PsA (Psoriatic arthritis) Tazarotene Duration of Remission: 1 year to decades Other Tx Salicylic Acid Tar III. SEBORRHEIC DERMATITIS (SD) NB-UVB (Narrowband UVB) 1st line: A. CLINICAL CASE 2 BB-UVB (Broadband UVB) Phototherapy 26-year-old female PUVA (Psoralen + Ultraviolet A) Other tx Onset: 2 years (recurrent) Excimer laser Similar lesions sometimes noted on the posterior auricular Methotrexate area, scalp, chest, and back Acitretin Apremilast Cyclosporine A Other agents: ○ Hydroxyurea ○ 6-thioguanine ○ Celicept ○ Sulfasalazine Biologics - injectables that restart immune Systemic system depending on target interleukins ○ Biologicals ○ Etanercept → Targets IL-36 and IL-23 Figure 30. Seborrheic dermatitis (Doc’s patient) ○ Adalimumab ○ Infliximab CHARACTERISTICS ○ Ustekinumab ○ Secukinumab Primary Lesion: Plaques, papules → Targets IL-17 – involved in psoriasis Secondary Lesion: Scales ○ Ixekizumab Skin Findings: ○ Multiple, erythematous papules and plaques Lecturer notes: ○ Well-demarcated Biologics → Can delineate the normal vs affected skin ○ Usually given to patients with psoriasis ○ Greasy scales over the forehead, nasolabial folds ○ Very expensive; ~₱400,000 for an entire cycle of tx → Indicate presence of sebum ○ Used when even systemic treatments i.e. oral or topical History: Sexual history and Past MHx (immune status) don’t work anymore B. GENERAL FEATURES Chronic and relapsing Usually affects adolescents and young adults (all ages) Increasing incidence in patients older than 50 years Infantile SD: peaks at 3 months old Male predominance Seasonal variation ○ Common and severe in the cold and dry climates, mitigated by sun exposure Can occur in: ○ Nasolabial folds ○ Posterior auricle Figure 29. Narrowband Phototherapy ○ Eyebrows MG 2 | MG 9 7 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS Associated with HIV/AIDS Uncontrolled multiple widespread lesions ○ More extensive and refractory patterns in up to 83% of and severe cases HIV-seropositive and AIDS patients Examples: ○ Usually in px that undergo retroviral therapy ○ Glucocorticoids (low doses) ○ Oral antifungals - given if systemic C. CLINICAL PRESENTATION treatment not effective Erythematous, scaly patches on sebaceous gland-rich sites: → Itraconazole (200 mg/day for first 7 ○ Scalp, face, upper trunk, and intertriginous area days each month) Severity varies from mild erythema and pruritus to severe, → Isotretinoin (0.1 - 0.5 mg/kg) oily, thick scale with a burning or tingling sensation ○ Starts as white to thick yellowish scales Lecturer notes: Steroids should NOT be given long-term INFANTILE SEBORRHEIC DERMATITIS ○ Steroid Holiday - discontinuation of steroid therapy Non-pruritic Stretch marks - caused by chronic long-term use of ○ However, infants cannot verbalize when they feel itchy steroids on the skin Most Common Areas: ○ Frontal or vertex areas (or both areas) of the scalp F. PROGNOSIS ○ Central areas of the face Table 4. Prognosis of Seborrheic Dermatitis (SD) Hallmark: “Cradle cap” Dry, thick adherent, and flaking scale AGE GROUP PROGNOSIS Usually with erythematous rash on intertriginous folds of the Adolescents & trunk and extremities Chronic and recurrent relapsing course Adults Resolves spontaneously within the first 6 to 12 months of life Benign, self-limited course D. ETIOLOGY AND PATHOGENESIS Spontaneously disappears by 6-12 Infantile SD months of age Etiology has not been clearly identified yet Does NOT progress to adulthood Role of sebaceous glands Immunologic status of patients (more common in AIDS and IV. PITYRIASIS ROSEA Parkinson's Disease) Causative agent: Malassezia (yeast) A. CLINICAL CASE 3 24-year-old male with 2 week onset associated with pruritus. E. MANAGEMENT Table 3. Infantile SD TREATMENT EXAMPLES Corticosteroids (mild potency formulations) 1st Line Calcineurin inhibitors Topical ○ Tacrolimus - act like steroids. Medications Antifungal drugs Keratolytics Emollients ○ Mineral oil ○ Vegetable oil ○ Petroleum jelly Figure 31. Pityriasis Rosea (PR) (upon onset) Soft rubbing with a brush or comb For Dandruff/Pityriasis Simplex Capillitia: ○ Shampoos containing zinc pyrithione, selenium sulfide, ketoconazole, salicylic acid, ciclopirox, and coal tar For Infantile SD: Others ○ Diaper areas: Superabsorbent disposable diapers with frequent changes Figure 32. PR 2 weeks after onset ○ Topical antifungal and anti-inflammatory 1. What is the primary and secondary lesion? ○ Secondary infection: Appropriate ○ Macules, papules, plaque, scales systemic drugs 2. What is this lesion called? (Referring to Figure 31) ○ NOT RECOMMENDED: ○ Herald patch → Soap and alcohol containing 3. What is the etiology of this disease? compounds ○ Human Herpes Virus (HHV) 6 and/or 7 → Keratolytic agents 4. What is the diagnosis? ○ Pityriasis rosea Systemic Usually NOT indicated unless it is very 5. What is the typical distribution of the rash? Therapies generalized and inflammation is chronic ○ Lines of cleavage MG 2 | MG 9 8 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS B. EPIDEMIOLOGY E. DIAGNOSIS Worldwide distribution All races 0.64 per 100 dermatologic patients Clustering of cases - infectious etiology Female > Male (1.39 : 1) Peak: 10-35 years C. CLINICAL FEATURES PRIMARY ERUPTION: HERALD PATCH Well-demarcated, thin, oval-to-round plaque that is usually pink, rose-colored, erythematous, or, less commonly hyperpigmented solitary lesion on the trunk or extremity ○ Trunk (50%) > extremity and neck Slightly depressed center and fine collarette of scale within periphery Figure 34. Diagnostic Criteria for PR (See Appendix) Atypical locations: dorsal feet, face, scalp, and genitalia 2-10 cm F. MANAGEMENT Isolated on ave. of 2 weeks in adults and 4 days in children Self-limited disease = no treatment is necessary SECONDARY ERUPTION Counseling and reassurance Associated pruritus: Topical steroids and antihistamines 2 weeks after the Herald patch (few hours-3 months) High-dose acyclovir (800mg, 5 times a day) Multiple, round-to-oval, 0.5-1.5 cm macules, papules, ○ Unclear mechanism plaques Ultraviolet B phototherapy Light pink with a fine collarette of scale Resemble herald patch in miniature G.CLINICAL COURSE AND PROGNOSIS Bilateral and symmetrical Self-resolves after an ave. of 45 days (2 weeks-5 months) Trunk and proximal extremities Persistent PR: >3 months, with rash Lines of cleavage: Christmas tree pattern ○ Treated with Acyclovir Post-inflammatory hyperpigmentation or hypopigmentation Recurrences can occur (uncommon) V. PITYRIASIS RUBRA PILARIS (PRP) A. CLINICAL CASE 4 A 58-year-old male Onset: 2 months Lesions started at the head spreading caudally. Figure 35. PRP 1. What is the primary and secondary lesion? ○ Macules, patches, papules 2. What is the diagnostic hallmark of this disease? Figure 33. Christmas Tree Distribution / Pattern in Pityriasis Rosea ○ “Nappes Claires”: sharply demarcated islands of normal skin D. ETIOLOGY AND PATHOGENESIS 3. What is the diagnosis? Infectious agent: ○ Pityriasis Rubra Pilaris (PRP) Type 1 ○ Case clustering 4. Other important clinical findings: ○ Possible seasonal variation ○ Erythroderma ○ Resemblance to other known exanthems ○ Palmoplantar hyperkeratosis ○ Presence of prodromal symptoms ○ Follicular hyperkeratosis ○ Human Herpes Virus 6 and /or 7 Cell-mediated immunity B. EPIDEMIOLOGY ○ Infiltrate of PR was predominantly T cells Rare inflammatory papulosquamous dermatosis, often ○ Increased CD4-to-CD8 ratio self-limiting within a few years ○ Increased proportion of Langerhans cells Affects all races Cytokine profile Male = female ○ Increased IL-17, interferon-gamma, vascular endothelial Mostly sporadic with unknown etiology growth factor, & interferon-inducible protein-10 (CXCL10) 6.5%: Familial (CARD14 mutations) MG 2 | MG 9 9 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS C. TYPES OF PRP TYPE I (CLASSIC ADULT) Most common subtype (>50% of cases) Starts with erythematous macules forming patches Follicular hyperkeratotic papules on upper half of body ○ Thickening of pores As disease evolves, yellow-orange, scaling dermatitis often spreads to generalized erythroderma over 2 to 3 months Type 1 Diagnostic Markers: Figure 38. Splinter Hemorrhages ○ Nappes Claires - diagnostic hallmark → Sharply demarcated islands of unaffected skin ○ Waxy diffuse, yellowish keratoderma (thickening) of the palms and soles ○ Nail plate thickening ○ Splinter hemorrhages ○ Subungual hyperkeratosis Figure 39. Subungual Hyperkeratosis TYPE II (ATYPICAL ADULT) 5% of PRP patients Characterized by its atypical morphologic picture and a long duration of more than 20 years Ichthyosiform scaling, areas of follicular hyperkeratosis Sparseness of the scalp hair Cephalocaudal progression in Type 1 is missing. Less tendency to develop erythroderma Similar to Type 1 but does not manifest erythroderma TYPE III (CLASSIC JUVENILE) Figure 36. Classic Adult Type I Pityriasis Rubra Pilaris. Note the Clinical counterpart of Type 1 in adult white islands of normal skin (Nappes Claires) 10% of PRP patients Onset: between the ages of 5 and 10 years Course: may be shorter with clearing after 1 year TYPE IV (CIRCUMSCRIBED JUVENILE) 25% or PRP patients Manifests in prepubertal children and young adults Well-demarcated hyperkeratotic erythematous plaques on elbows and knees Do not progress or widespread to other areas Palmoplantar Keratoderma – characteristic of Type 4 but may also be absent Figure 37. Palmar (A) and Plantar (B) “waxy” Keratoderma in PRP Figure 40. Well-Demarcated Hyperkeratotic Erythematous Figure 37. Nail Plate Thickening Plaques, Mimicking Psoriasis (PRP Type IV) MG 2 | MG 9 10 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS F. MANAGEMENT Table 5. Management of PRP Emollients (water-in-oil emulsion) TOPICAL Keratolytics (salicylic acid, urea) Vitamin D3 (calcipotriol) Retinoids (0.5-0.75 mg/kg 1ST LINE acitretin/day) Methotrexate (10-25 mg weekly SYSTEMIC or higher) Antiretroviral therapy (HIV-associated variant) Glucocorticoids (medium to high Figure 41. Palmoplantar Keratoderma in Type IV PRP TOPICAL potency) Vitamin A analogs (tazarotene) Photochemotherapy (topical or systemic PUVA) UVA1 phototherapy PHYSICAL UVB (narrowband) phototherapy UVB phototherapy Extracorporeal photopheresis 2ND LINE TNF-antagonists Anti-IL-12/ IL-23p40 ustekinumab Anti-IL17 SYSTEMIC Azathioprine (100-150 mg/day) Fumaric acid esters Cyclosporine (5 mg/kg/day) Figure 42. Palmoplantar Keratoderma Apremilast TYPE V (ATYPICAL JUVENILE) G. PROGNOSIS 5% of patients Early age of onset and a chronic course Table 6. Prognosis of PRP Most patients of the familial PRP belong to this category TYPE PROGNOSIS Mutation in the CARD14 gene Hyperkeratotic follicular lesions I Resolves within 3 years May present with scleroderma-like features affecting hands and feet II Less-favorable prognosis for remission III Resolves within 1-2 years TYPE VI (HIV-ASSOCIATED) IV Less-favorable prognosis for remission Similar with Type 1 – with variable beginning Follicular papules and prominent follicular plugging V Little or no tendency to resolve spontaneously Symmetrically distributed lesions of the extensor surfaces frequently progress to erythroderma VI. PARAPSORIASIS Additional manifestations: ○ Acne conglobata A. CLINICAL CASE 5 ○ Hidradenitis suppurativa ○ Lichen spinulosus A 51-year-old male is asymptomatic to mildly pruritic. D. ETIOLOGY AND PATHOGENESIS Unknown Proposed pathogenic mechanisms: ○ Upper Respiratory Tract Infection (URTI) ○ HIV Type V PRP: CARD 14 gene mutation E. DIAGNOSIS Clinical Biopsy to differentiate from psoriasis Figure 43. Small Plaque Parapsoriasis MG 2 | MG 9 11 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS Figure 44. Large Plaque Parapsoriasis 1. What is the primary and secondary lesion? Figure 45. Retiform (left) & Poikilodermatous (right) Variants ○ Patches 2. Where is the common area of distribution of lesions? C. SMALL PLAQUE PARAPSORIASIS ○ Bathing trunk 3. What is the diagnostic hallmark of this disease? ○ Cigarette-paper wrinkling 4. What is the diagnosis? ○ Large Plaque Parapsoriasis B. LARGE PLAQUE PARAPSORIASIS EPIDEMIOLOGY Middle-aged and older people Peak: 5th decade Male predominance Affects all racial groups and geographic regions CLINICAL FEATURES Figure 46. Small Plaque Parapsoriasis Salmon pink, oval or irregularly shaped patches or very thin (Digitate Dermatosis Variant) plaques About Figure 45: Asymptomatic or mildly pruritic ○ Small plaque parapsoriasis can look like a hug that left Well-marginated fingerprints on the trunk. > 5cm Location: bathing trunk and flexural areas CLINICAL FEATURES Lesions may appear finely wrinkled – “cigarette paper” wrinkling “Chronic superficial dermatitis” Asymptomatic round or oval discrete patches or very thin VARIANTS plaques, covered with fine, moderately adherent scales ○ Can sometimes be a pruritic (itching) disease Table 5. Variants of Large Plaque Parapsoriasis ○ Scaling VARIANT DESCRIPTION Mainly on the trunk Lesions → Less than 5 cm in diameter Rare Variant: Digitate Dermatosis Presents with extensive eruption of ○ Usually seen as a “hug that left fingerprints on trunk” Retiform scaly macules and papules in a net-like or zebra-stripe pattern D. ETIOLOGY AND PATHOGENESIS Eventually becomes poikilodermatous Triad: ○ Mottled pigmentation ○ Atrophy Poikilodermatous ○ Telangiectasia Aka Poikiloderma Atrophicans Vasculare Figure 47. Etiology and Pathogenesis of Small Plaque Parapsoriasis MG 2 | MG 9 12 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS About Figure 47: ○ Etiology is still unknown ○ From Chronic Dermatitis → may evolve into Cutaneous T-cell Lymphoma, e.g. Mycosis Fungoides ○ Theory: parapsoriasis would bridge these two conditions. → Possibly because parapsoriasis stimulates T-cell (SALT), which aids in T-cell lymphoma development E. MANAGEMENT Table 7. Management of Parapsoriasis 1ST LINE 2ND LINE Emollients Topical bexarotene Topical corticosteroids Topical imiquimod Topical tar products Psoralen and UVA Figure 48. Pityriasis Lichenoides et Varioliformis Acuta (PLEVA) Sunbathing Topical mechlorethamine Broadband UVB Topical carmustine (BCNU) phototherapy Excimer laser (308 nm) Narrowband UVB phototherapy Low-dose ultraviolet A1 (UVA1) Table 8. Small Plaque Parapsoriasis vs. Large Plaque Parapsoriasis SMALL PLAQUE LARGE PLAQUE PARAPSORIASIS PARAPSORIASIS (SPP) (LPP) Figure 49. Pityriasis Lichenoides et Varioliformis Acuta (PLEVA) Reassured and may forego Aggressive therapy Upon Close Inspection treatment Goal: 1. What are the primary and secondary lesions? Initially examined every 3-6 ○ Suppress and prevent ○ Papules and pustules (primary) months and subsequently possible progression to ○ Crust, ulcers (secondary) every year overt MF (Mycosis 2. What is the diagnosis? fungoides) ○ Pityriasis Lichenoides et Varioliformis Acuta (PLEVA) Examine every 3 months 3. What is the commonly associated complication? initially and every 6 months ○ Secondary infection to 1 year subsequently for evidence of progression B. EPIDEMIOLOGY Repeated multiple biopsies of suspicious lesions All racial and ethnic groups Children and Young Adults F. PROGNOSIS Fall and winter Both small plaque parapsoriasis and large plaque Male > Female (1.5:1 to 3:1) parapsoriasis may persist for years to decades with little PLC > PLEVA (3-6x) change in appearance 10-30% large plaque parapsoriasis to overt Mycosis fungoides C. CLINICAL FEATURES Retiform variant large plaque parapsoriasis to Mycosis fungoides in most cases Table 9. Clinical Features of PLC and PLEVA Small plaque parapsoriasis is clinically benign PLC PLEVA Recurrent crops of Recurrent crops of VII. PITYRIASIS LICHENOIDES erythematosus, scaly erythematous papules that Pityriasis Lichenoides et varioliformis acuta (PLEVA) papules that develop crusts, vesicles, Pityriasis Lichenoides Chronica (PLC) spontaneously regresses pustules, or erosion over several weeks to before spontaneously A. CLINICAL CASE 6 months regressing within a matter of weeks An 18-year-old male Distribution: trunk and extremities Lesions tend to concentrate on the trunk and proximal Manifestations: (+) pruritus, low-grade fever, body malaise, extremities, but any region of the skin, even mucous arthralgia membranes, can be involved History: Same lesions in the past but noted resolution Characteristic lesion: various stages of evolution with a polymorphous appearance MG 2 | MG 9 13 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS ○ Polymorphic - presents different configuration / features ○ Can develop high fever, malaise, myalgia, arthralgia, (e.g. mixture of big & small size lesions, different colored gastrointestinal, and central nervous system lesions) symptoms which can occasionally be fatal Figure 50. Pityriasis Lichenoides et Varioliformis Acuta (PLEVA) Figure 53. Purpuric Papulonodules with Central Ulcers About Figure 51: ○ Ulceronecrotic, hyperacute variant ○ Large necrotic eschar with halo erythema developing in a febrile patient with antecedent pityriasis lichenoides et varioliformis acuta E. ETIOLOGY AND PATHOGENESIS Etiology is unknown Associated with: ○ Infectious agents: Toxoplasma gondii, Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, parvovirus B19, Figure 51. Pityriasis Lichenoides et Varioliformis Acuta (PLEVA) human herpesvirus-8, and HIV ○ Estrogen-progesterone therapy, chemotherapy drugs, radiocontrast iodide, and influenza vaccine ○ HMG-CoA reductase inhibitors F. DIAGNOSIS Clinical Nonspecific blood abnormalities: ○ Leukocytosis ○ Decreased CD-4:CD-8 ratio Histopathology Figure 52. Pityriasis Lichenoides et Varioliformis Acuta (PLEVA) F. MANAGEMENT About Figures 50, 51, 52: Table 10. Management of Pityriasis Lichenoides ○ 50: Adolescent with multiple erythematous papules and 1ST LINE SECOND LINE crusted lesions in various stages of evolution. ○ 51: Larger papulovesicular and hemorrhagic, crusted Topical corticosteroid + Topical Tacrolimus lesions in an adult. Note varioliform scars adjacent to active phototherapy Prednisone lesions on posterior thigh and leg. Antibiotics - for 60/40/20 PO taper, 5 days ○ 52: Pustules, crusts, and necrotic centered papules with anti-inflammatory each erythematous, indurated bases. ○ Erythromycin: Methotrexate: 500 mg PO 2-4x daily 10 - 25 mg PO weekly D. COMPLICATIONS ○ Tetracycline: Phototherapy: 500 mg PO 2-4x daily UVA173, psoralen + UVA69 Most common: Secondary infection ○ Minocycline: Cyclosporine: PLEVA: low-grade fever, malaise, headache, and arthralgia 100 mg twice daily 2.5-4 mg/kg/day total dose (joint stiffness) ○ Azithromycin: divided into twice daily, PO PLC: associated uncommonly with LPP (large plaque 500 mg PO on day 1 doses; use the minimum parapsoriasis) in children and 250 mg on days Retinoids: Very rarely: Mycosis Fungoides 2-5 bimonthly eg/ acitretin 25 - 50 mg PO PLEVA variant: Pityriasis lichenoides with ulceronecrosis and For acute and severe daily hyperthermia (PLUH) / Febrile ulceronecrotic cases: Systemic therapy Photodynamic therapy Mucha-Habermann disease (FUMHD) Bromelain (pineapple extract) MG 2 | MG 9 14 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS VIII. EXERCISES CASE #4 CASE #1 1. Identify the nail finding? ○ Hyperkeratosis/Subungual Hyperkeratosis CASE #5 1. What is the predominant primary lesion? ○ Plaque 2. What is the specific diagnosis? ○ Erythrodermic Psoriasis 3. What is the prominent feature of this case? ○ Erythroderma 4. Topical treatment? ○ Corticosteroids 5. Systemic treatment? ○ Methotrexate ○ Isotretinoin ○ Other Biologics CASE #2 1. What is the diagnosis? ○ Seborrheic Dermatitis 2. First line of treatment? ○ Corticosteroids ○ Calcineurin inhibitors ○ Antifungal drugs ○ Keratolytics 3. Highly associated with what condition? ○ HIV/AIDS, Immunocompromised state CASE #6 1. Identify the nail finding? ○ Nail pitting 2. What is the probable cause? ○ Defective keratinization CASE #3 1. Identify the nail finding? 1. What is the specific diagnosis? ○ Oil Spots/Salmon Spots ○ Infantile Seborrheic Dermatitis (ISD) MG 2 | MG 9 15 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS CASE #7 ○ Guttate - small, drop-shaped lesions. ○ Small Plaque - tiny plaques, similar to plaque psoriasis but smaller. ○ Inverse - smooth, red patches in skin folds (e.g., armpits, groin). ○ Erythrodermic - widespread redness and shedding of the skin. ○ Pustular - white pustules surrounded by red skin. → General Pustular Psoriasis (von Zumbusch type) Acute Usually preceded by other forms of the disease Fever + sudden generalized eruption of sterile 1. What is the diagnosis? pustules ○ Pityriasis rosea Areas affected: Trunks and extremities, nail beds, 2. These same lesions persisted for 3 months, what is your palms, and soles diagnosis? Provoking agents: Infections, irritating topical ○ Persistent pityriasis rosea treatment, corticosteroid withdrawal 3. What is the etiology? Complications: Hypocalcemia, bacterial ○ HHV-6 and 7 superinfection, sepsis, dehydration → Annular Pustular Psoriasis - annular/circinate lesion CASE #8 → Impetigo Herpetiformis Onset: 3rd trimester Can resolve or develop/progress into psoriasis → Pustulosis Palmaris et Plantaris Areas affected: Palms and soles → Acrodermatitis Continua of Hallopeau (Dermatitis Repens) - causes osteolysis ○ Sebopsoriasis - overlap of psoriasis and seborrheic dermatitis; red, scaly patches on scalp, face, and chest. ○ Napkin Psoriasis - diaper area of infants; red, sharply demarcated rash. ○ Linear Psoriasis - psoriatic lesions arranged in a linear pattern, following lines of trauma or injury (Koebner phenomenon). 1. What is the specific diagnosis? Nail Changes in Psoriasis ○ Pustular psoriasis ○ Nail pitting 2. Aside from infection, give 1 provoking factor? → One of the most common features of psoriasis ○ Withdrawal of systemic corticosteroids → Cause: defective keratinization 3. Give 1 complication? → If >20 pits on the 10 digits = (+) psoriasis ○ Hypocalcemia ○ Oil spots/Salmon spots/Candle dripping ○ Bacterial superinfection → Characterized as translucent, yellow-red ○ Sepsis discolorations observed beneath the nail plate often ○ Dehydration extending toward the hyponychium → Caused by psoriasiform hyperplasia, parakeratosis, VIII. SUMMARY microvascular changes, and trapping of neutrophils in Papulosquamous Reaction Pattern nail bed ○ Primary lesion - relatively thin/flat-topped papule/plaque ○ Onycholysis with scale → Separation of nail plate from nail bed ○ Crust or lichenification Lysis of nails (onycho-) ○ Involve the epidermis and superficial to mid-dermis → Usually involves distal aspect of the nails Psoriasis Vulgaris ○ Onychodystrophy ○ Primary: Plaques/Papules → Nails are dystrophic ○ Secondary: Scales → Stronger association with psoriatic arthritis ○ Skin findings: Multiple erythematous papules and scaly Very debilitating plaques over the trunk and extremities. ○ Psoriatic Arthritis ○ Important physical findings: Nails → Seen in 40% of the patients Epidemiology of Psoriasis → Has a strong genetic component or predisposition ○ Worldwide occurrence → Manifestations involves peripheral arthritis, ○ Prevalence: 0.1%-3% spondyloarthritis, enthesitis, and dactylitis ○ Males = Females → Nail disease: known risk factor (80%) ○ Age on onset = 15-30 years old → No topical treatment ○ Multifactorial inheritance ○ Known Complications of Psoriatic Arthritis ○ Polygenic + Environmental → Increased morbidity & mortality from cardiovascular Types of Psoriasis events ○ Plaque - raised, red patches with silvery scales. → Myocardial infarction MG 2 | MG 9 16 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS Most common complication Celicept → Metabolic syndrome (x 2.9) Sulfasalazine → Rheumatoid arthritis → Biologics - injectables that restart the immune system → Crohn’s disease and ulcerative colitis depending on which interleukins are being targeted → Hodgkin’s lymphoma Biologicals → Cutaneous T-cell lymphoma Etanercept → Depression and anxiety ⎻ Targets IL-36 and IL-23 ○ Pathogenesis Adalimumab → Both external environmental factors and intrinsic Infliximab genetic susceptibility factors Ustekinumab → Cutaneous immune system plays a central role Secukinumab ○ Risk Factors ⎻ Targets IL-17 which is involved in psoriasis → Obesity Ixekizumab → Heavy smoking (>20 cigarettes daily) Prognosis of Psoriasis ○ Younger age of onset and positive family history Also includes vaping ○ Guttate psoriasis = self-limited → Infections (i.e., Streptococcal throat infections, HIV ○ Chronic plaque psoriasis = lifelong disease infection, Hepatitis C infection) ○ Erythrodermic and generalized pustular psoriasis → Drugs: antimalarials, B blockers, lithium, nonsteroidal → Severe and persistent prognosis anti-inflammatory drugs (NSAIDs), IFNs-alpha and ○ Frequently relapsing gamma, imiquimod, angiotensin-converting enzyme ○ A history of onset of joint symptoms: inhibitors, and gemfibrozil → Before the 4th decade ○ Diagnosis → History of warm, swollen joints → Clinical Diagnosis → Should raise the suspicion of PsA (Psoriatic arthritis) However, sometimes we can see cases where it ○ Duration of remission: 1 year to decades doesn’t fit the criteria for psoriasis Seborrheic Dermatitis → Histopathology ○ General features: Done when we’re doubtful of our initial/working → Chronic and relapsing diagnosis → Usually affects adolescents and young adults Sometimes, we tend to underestimate the cases, → Infantile SD: peaks at 3 months old but when we examine via the microscope, it’s → Male predominance something completely different → Common and severe in the cold and dry climates Clinical Variants of Pustular Psoriasis → Associated with HIV/AIDS ○ Generalized pustular psoriasis (von Zumbusch type) ○ Skin findings → Widespread pustules, fever, systemic symptoms, → Multiple, erythematous papules and plaques life-threatening. → Well-demarcated ○ Annular pustular psoriasis You can delineate the normal vs affected skin → Ring-shaped lesions with pustules around the edge, → Greasy scales over the forehead, nasolabial folds less severe than generalized forms. Indicate presence of sebum ○ Impetigo herpetiformis ○ Clinical Presentation → Pustular psoriasis during pregnancy, systemic → Erythematous, scaly patches on sebaceous involvement, risk for both mother and fetus. gland-rich sites ○ Pustulosis palmaris et plantaris → Severity varies from mild erythema and pruritus to → Pustules on palms and soles, often chronic and severe, oily, thick scale recurrent. → Infantile SD ○ Acrodermatitis continua of Hallopeau Non-pruritic → Pustules on fingertips and nails, may lead to nail “Cradle cap” destruction, chronic and relapsing. Resolves spontaneously within the first 6 to 12 Treatment of Psoriasis months of life ○ Topical treatments ○ Etiology and Pathogenesis → 1st line: Emollients, Steroids, Vitamin D3 Analogs, → Etiology has not been clearly identified yet Calcineurin Inhibitors → Role of sebaceous glands → Other Tx: Tazarotene, Salicylic Acid, Tar → Immunologic status of patients (more common in AIDS ○ Phototherapy and Parkinson's Disease) → 1st line: NB-UVB (Narrowband UVB), BB-UVB → Causative agent: Malassezia (yeast) (Broadband UVB) ○ Management → Other tx: PUVA (Psoralen + Ultraviolet A), Excimer laser → 1st line: Topical medications ○ Systemic treatments → Emollients → Methotrexate → Soft rubbing with a brush or comb → Acitretin → For dandruff or Pityriasis simplex capillitia: → Apremilast Shampoos containing zinc pyrithione, selenium → Cyclosporine A sulfide, ketoconazole, salicylic acid, ciclopirox, and → Other agents: coal tar Hydroxyurea → Systemic therapies - usually NOT indicated unless it is 6-thioguanine very generalized and the inflammation is chronic MG 2 | MG 9 17 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS → For Infantile SD Onset: between the ages of 5 and 10 years Diaper areas: Superabsorbent disposable diapers Course: may be shorter with clearing after 1 year with frequent changes → Type IV (Circumscribed Juvenile) Topical antifungal and anti-inflammatory 25% or PRP patients Secondary infection: Appropriate systemic drugs Characterized by well-demarcated NOT RECOMMENDED: hyperkeratotic erythematous plaques on the ⎻ Soap and alcohol containing compounds elbows and knees ⎻ Keratolytic agents Palmoplantar keratoderma: Characteristic of Type ○ Prognosis 4 but may also be absent → Adolescents & Adults: → Type V (Atypical Juvenile) Chronic and recurrent relapsing course 5% of patients → Infantile SD: Early age of onset and a chronic course Benign, self-limited course Mutation in the CARD14 gene Spontaneously disappears by 6-12 months of age Hyperkeratotic follicular lesions Does NOT progress to adulthood → Type VI (HIV-associated) Pityriasis Rosea Similar with Type 1 – with variable beginning ○ Worldwide distribution Follicular papules and prominent follicular ○ Female > Male (1.39 : 1) plugging ○ Peak: 10-35 years ○ Etiology and Pathogenesis ○ Clinical Presentation → Unknown → Primary eruption: Herald Patch → Proposed pathogenic mechanisms Well-demarcated, thin, oval-to-round plaque Upper Respiratory Tract Infection (URTI) Slightly depressed center and fine collarette of HIV scale within the periphery → Type V PRP: CARD 14 gene mutation Trunk (50%) > extremity and neck ○ Diagnosis 2-10 cm → Clinical → Secondary eruption → Biopsy to differentiate from psoriasis 2 weeks after the Herald patch (few hours-3 ○ Management months) → 1st line Resemble herald patch in miniature Topical: Emollients, Keratolytics, Vitamin D3 Lines of cleavage: Christmas tree pattern Systemic: Retinoids, Methotrexate, Antiretroviral ○ Etiology and Pathogenesis therapy → Infectious agent: Human Herpes Virus 6 and /or 7 → 2nd line → Cell-mediated immunity Topical: Glucocorticoids, Vitamin A analogs → Cytokine profile Physical: Photochemotherapy, UVA1, UVB ○ Management (narrowband), UVB, Extracorporeal photopheresis → Self-limited disease = no treatment is necessary Systemic: TNF-antagonists, Anti-IL-12/ IL-23p40 → Associated pruritus: Topical steroids and ustekinumab, Anti-IL17, Azathioprine , Fumaric acid antihistamines esters, Cyclosporine, Apremilast → High-dose acyclovir (800mg, 5 times a day) – unclear → Prognosis mechanism Type I: Resolves within 3 years ○ Clinical Course and Prognosis Type II: Less-favorable prognosis for remission → Self-resolves after an average of 45 days (2 weeks-5 Type III: Resolves within 1-2 years months) Type IV: Less-favorable prognosis for remission → Persistent PR: >3 months, with rash Type V: Little or no tendency to resolve Treated with Acyclovir spontaneously Pityriasis Rubra Pilaris (PRP) Parapsoriasis ○ Rare inflammatory papulosquamous dermatosis, often ○ Large Plaque self-limiting within a few years → Middle-aged and older people ○ Male = female → Peak: 5th decade ○ Types → Male predominance → Type I (Classic Adult) → Clinical Features Most common subtype (>50% of cases) Salmon pink, oval or irregularly shaped patches or Starts with erythematous macules forming very thin plaques patches Asymptomatic or mildly pruritic Nappes Claires - diagnostic hallmark Lesions may appear finely wrinkled – “cigarette → Type II (Atypical Adult) paper” wrinkling 5% of PRP patients → Variants Characterized by its atypical morphologic picture Retiform and a long duration of more than 20 years ⎻ Presents with extensive eruption of scaly Similar to Type 1 but does not manifest macules and papules in a net-like or erythroderma zebra-stripe pattern → Type III (Classic Juvenile) Poikilodermatous Clinical counterpart of Type 1 in adult ⎻ Mottled pigmentation 10% of PRP patients ⎻ Atrophy MG 2 | MG 9 18 of 21  Y2B10M1L5: COMMON PAPULOSQUAMOUS SKIN DISORDERS ⎻ Telangiectasia HMG-CoA reductase inhibitors ⎻ Extensive eruption of scaly macules and ○ Diagnosis papules in a net-like or zebra-stripe pattern → Clinical ○ Small Plaque → Nonspecific blood abnormalities → Clinical Features → Histopathology “Chronic superficial dermatitis” ○ Management Asymptomatic round or oval discrete patches or → 1st line very thin plaques, covered with fine, moderately Topical corticosteroid + phototherapy adherent scales Antibiotics: Erythromycin, Tetracycline, Minocycline, ○ Etiology and Pathogenesis Azithromycin → Etiology is still unknown For acute and severe cases: Systemic therapy → From Chronic Dermatitis → may evolve into → 2nd line: Topical tacrolimus, Prednisone, Methotrexate, Cutaneous T-cell Lymphoma, e.g. Mycosis Cyclosporine, Retinoids, Photodynamic therapy, Fungoides Bromelain ○ Management → 1st line: Emollients, Topical corticosteroids, Topical tar IX. REVIEW QUESTIONS products, Sunbathing, Broadband UVB phototherapy, Narrowband UVB phototherapy, Low-dose ultraviolet 1. Which of the following is a known complication of Generalized A1 (UVA1) Pustular Psoriasis (von Zumbusch type)? → 2nd line: Topical bexarotene, Topical imiquimod, A. Hypercalcemia Psoralen and UVA, Topical mechlorethamine, Topical B. Hypocalcemia carmustine (BCNU), Excimer laser (308 nm) C. Viral superinfection → SPP D. Pulmonary embolism Initially examined every 3-6 months and E. Hypoglycemia subsequently every year 2. Which of the following is FALSE of inverse psoriasis? → LPP A. It commonly presents with extensive scaling and flaking. Aggressive therapy B. It is localized in major skin folds, such as the axillae and Suppress and prevent possible progression to overt genitocrural region. MF (Mycosis fungoides) C. Scaling is usually minimal or absent. ○ Prognosis D. Sweating may be impaired in affected areas. → Both small plaque parapsoriasis and large plaque 3. Which of the following is TRUE about plaque-type psoriasis? parapsoriasis may persist for years to decades with A. The lesions are primarily found on the flexor surfaces of the little change in appearance extremities. → Small plaque parapsoriasis is clinically benign B. The Auspitz sign refers to pin-point bleeding after forcible Pityriasis Lichenoides removal of the outer scales. ○ Children and Young Adults C. The Koebner phenomenon is the spontaneous resolution ○ Male > Female (1.5:1 to 3:1) of psoriatic lesions. ○ PLC > PLEVA (3-6x) D. Plaque-type psoriasis is characterized by diffuse erythema ○ Clinical Features without scaling. → Pityriasis Lichenoides Chronica (PLC) Recurrent crops of erythematosus, scaly papules 4. Which of the following statements is TRUE about that spontaneously regresses over several erythrodermic psoriasis? weeks to months A. It is localized to the upper trunk and proximal extremities. → Pityriasis Lichenoides et varioliformis acuta B. Erythema is the most prominent feature, and patients are (PLEVA) at risk for hypothermia. Recurrent crops of erythematous papules that C. It primarily presents as small papules and is associated develop crusts, vesicles, pustules, or erosion with Streptococcal throat infection. before spontaneously regressing within a matter D. Scaling is thick and extensive in affected areas. of weeks 5. True or False: Seborrheic dermatitis is characterized by ○ Characteristic lesion: various stages of evolution with a plaques that extend beyond the hairline, while sebopsoriasis polymorphous appearance affects only the scalp. ○ Complications 6. Seborrheic dermatitis is a common skin condition that can → Most common: Secondary infection affect various age groups. Which of the following statements → PLEVA: low-grade fever, malaise, headache, and about seborrheic dermatitis is TRUE? arthralgia (joint stiffness) A. It exclusively affects patients older than 50 years. → PLC: associated uncommonly with LPP (large plaque B. Seborrheic dermatitis occurs equally in both men and parap