Video 17º Clase 2026 Psoriasis - Módulo de DERMATOLOGIA

Main Ideas, Concepts, and Lessons

1) What Psoriasis Is

• Psoriasis is a chronic, systemic, polygenic, multifactorial inflammatory disease.
• Genetics + triggers lead to abnormalities across:
  • Biochemical
  • Vascular
  • Immune systems
• These processes culminate in formation of the psoriasis plaque.

2) Epidemiology and Genetic Predisposition

• Global prevalence: ~2% (noted as “relative” across literature)
• Age-of-onset peaks (with variability in reports):
  • ~20–30 years (some literature suggests 40–50)
  • ~50–60 years
• Family history (first-degree relatives): roughly 30–90% of patients report it
• Genetics: about 15 gene types/variants described (examples):
  • Type 1 / juvenile psoriasis: associated with HLA-C6 (“HLAC6”)
    • described as more severe; occurs under 40
  • Arthritis subtype: associated with HLA-B27

3) Triggers (Internal and External)

• Internal triggers:
  • Alcohol consumption
  • Obesity
  • Smoking
  • Certain drugs (e.g., beta-blockers, lithium-containing drugs)
  • Stress
  • Streptococcal infections
  • Viral infections
• External triggers:
  • Radiation
  • Viral infections
  • Trauma (lesion induction after injury—ties into the Koebner/Köbner phenomenon)

4) Core Pathophysiology (Cascade Concept)

• Central idea: keratinocytes and immune activation create a self-amplifying inflammatory loop.
• Mechanistic sequence (as described):
  1. Genetic predisposition + triggers activate dendritic cells
  2. Basal keratinocyte signals alert local lymphocytes to keratin acting as a “self-antigen”
  3. A cytokine cascade begins
  4. T-cell polarization/activation produces responses:
     • TH1 / TH17 / TH22
  5. Epidermal changes: increased epidermal thickness
  6. Dermal vascular/inflammatory changes:
     • Vasodilation
     • Arrival of inflammatory cells
     • Elongation of dermal papillae
  7. Outcome: formation of the psoriasis plaque

5) Clinical Diagnosis (How It’s Recognized)

• Diagnosis is primarily clinical: detection of the typical plaque.
• Typical plaque features:
  • Erythematous (“salmon” / “chamois” tone) plaque
  • Well-defined borders
  • Silvery-white adherent scales
• Office confirmation:
  • Methodical scraping (Brock method) with three signs:
    • Stearin candle sign: flakes detach
    • Unfolding membrane sign: a membrane-like layer peels
    • Auspitz / bleeding dew sign: pinpoint bleeding from dilated dermal capillaries

6) Classification of Psoriasis (Multiple Axes)

• By age of onset:
  • Type 1 / juvenile: under 40, linked to HLA-C6, more severe
  • Type 2 / adult: 40–60, weaker HLA association
• By clinical pattern:
  • Cutaneous-only vs cutaneous + extracutaneous involvement
• By morphology/location (cutaneous examples):
  • Plaque psoriasis (vulgaris): ~80–90%
    • erythematous flaky plaques on extensor surfaces (e.g., knees)
  • Guttate psoriasis:
    • small plaques 0.5–1 cm
    • chest/limbs; often in children/adolescents; associated with streptococcal infection
  • Small plaque psoriasis:
    • small erythematous-chamois plaques 1.5–3 cm
  • Inverse psoriasis:
    • more erythema with scaling in folds (e.g., inguinal)
  • Pustular psoriasis variants:
    • includes annular and generalized
    • Generalized pustular psoriasis: an indication for hospitalization due to systemic compromise (fever, malaise, arthralgia)
  • Palmoplantar psoriasis: palms/soles
  • Erythrodermic psoriasis:

    • 80% BSA involved

    • diffuse erythema + scaling; no healthy skin patches
    • hospitalization indicated
  • Nail involvement: pits (nail pitting) and other nail changes
  • Ocular involvement: mentioned as systemic risk (to be elaborated later)

7) Differential Diagnoses (What to Distinguish From)

• Plaque psoriasis vs:
  • Tinea corporis (e.g., tinea / Trichophyton rubrum): raised circinate border with surface scale
  • Pityriasis rosea: identified by chronology including herald (mother) plaque
  • Cutaneous lymphomas (e.g., mycosis fungoides)
  • Subacute cutaneous lupus
  • Erythema / syphilitic lesions: described as “great imitator”
  • Erythrodermic causes: atopic dermatitis, drug reactions, lymphomas such as Sézary syndrome
• Small plaque psoriasis vs:
  • Nummular eczema
• Inverse psoriasis vs:
  • Candidal infection
  • Erythrasma (Corynebacterium)
  • Nummular eczema / lichen simplex chronicus (mentioned)
• Erythrodermic psoriasis vs other erythrodermas: examples above

8) Severity Scoring and Treatment Thresholds

• Clinical scoring guides severity and treatment intensity.
• Rule noted: palm area = 1% BSA (clarified as “palm only”).
• Score categories mentioned:
  • BSA (“BCA” as spoken):
    • Palm = 1% of body surface
    • Mild: 1–3%
    • Moderate: 3–10%
    • Severe: >10%
  • PASI: measures extent and lesion characteristics (scaling, infiltration, erythema)
  • DLQI: patient questionnaire for quality-of-life impact
• “Rule of 10” concept (as described):
  • If PASI + DLQI + BSA yields a value >10 → treat as moderate-to-severe and likely require systemic treatment
• Systemic risk link: moderate/severe psoriasis is associated with higher cardiovascular risk factors

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Comorbidities (Main Message and Mechanism)

1) Frequency

• 60–70% of psoriasis patients have at least one comorbidity
• Around 30% have three or more comorbidities

2) Why Comorbidities Occur (Mechanisms)

Comorbidities arise via multiple pathways:

• Shared inflammatory mechanisms (systemic inflammation)
• Persistent T-lymphocyte activation
• Systemic chronic inflammation (psoriasis is not “only skin”)
• Quality-of-life changes leading to behavioral/toxic habits
• Long-term treatments, including immunosuppressants

3) Inflammatory Mediator Pathway (Targets)

• Mediators increased in psoriasis plaque also rise in bloodstream.
• Actions described on three targets:
  • Liver
  • Adipose tissue
  • Skeletal muscle
• Mediators named:
  • TNF-α, IFN-α, IFN-γ
  • Interleukins 1, 6, 17

4) Metabolic/Vascular Complications (Cardiovascular Risk Model)

• Liver effects:
  • Increased homocysteine → endothelial damage
  • Increased C-reactive protein (CRP)
  • Increased fibrinogen → pro-thrombotic tendency
• Adipose tissue effects:
  • Release of adipokines (e.g., leptin, resistin, chimerin) →
    • worse lipid metabolism (↑ triglycerides, ↑ LDL)
• Skeletal muscle effects:
  • Blockage of glucose receptors → insulin resistance
  • Pancreatic overwork → increased risk of type 2 diabetes
• Endothelial/cardiovascular consequences:
  • Inflamed, rigid endothelium with loss of elasticity
  • Hypertension
  • Pro-thrombotic substances → atherosclerotic plaques
  • Risk of myocardial infarction, stroke, and other vascular disease

5) Emphasis on IL-6 and IL-17

• Later treatments target these pathways (“latest/popular treatments directed at these targets”).

6) Metabolic Syndrome and Cardiovascular Risk (Key Numbers)

• Hypertension prevalence:
  • ~32–38% overall in psoriasis
  • up to ~70% in severe psoriasis
• Obesity prevalence: ~30–40%
• Fatty liver: 1.5–3x higher chance
• Dyslipidemia: ~40%
• Type 2 diabetes: ~10–20%
• In a 2009 retrospective service study:
  • 36% had metabolic syndrome
  • 22 patients studied
  • Many overweight; nearly half obese
• Cardiovascular risk factor overview:
  • ~7/10 psoriasis patients have a cardiovascular risk factor
  • Modifiable factors: smoking, BP, obesity, diabetes, dyslipidemia
  • Smoking reported as the most prevalent risk factor
• Additional claims mentioned:
  • Severe psoriasis increases cardiovascular risk by 1.5 every 10 years
  • Heart attack earlier by ~5 years vs general population
  • Reduced survival by ~3 years (men) and 4 years (women)
  • Includes sudden death, heart failure, peripheral arterial disease

7) Other Associated Conditions

• Inflammatory bowel disease (IBD):
  • Shared genetic predisposition mentioned (chromosome 6p21)
  • IBD may occur concurrently or be influenced by therapy
  • Examples given:
    • Crohn’s disease: ~9.6% develop psoriasis or have psoriasis (wording slightly unclear)
    • Psoriasis patients:
      • ~2.5x more likely to develop Crohn’s disease
      • ~1.6x more likely to develop colitis
  • Shared response to immunomodulators mentioned (e.g., methotrexate)
  • Anti-IL-17 therapies may worsen IBD
• Ocular involvement / uveitis:
  • Differences depending on joint involvement:
    • psoriasis-only ocular disease: anterior uveitis
    • usually bilateral, refractory, recurrent; often needs systemic treatment including biologics
• Urethritis:
  • Associated with psoriasis; not always tied to arthropathy
  • Probability increases with arthropathy and with axial involvement
• Psoriatic arthropathy (seronegative):
  • HLA-B27-related seronegative arthropathy
  • Present in 6–42% of psoriasis patients
  • More common in severe psoriasis
  • Usually occurs ~10 years after cutaneous disease (but not always)
  • Nail involvement should raise suspicion for future joint involvement
  • Scalp involvement and inverse/fold psoriasis may coexist with joint symptoms
  • Patterns described:
    • Oligoarticular, or symmetric polyarthritis
    • distal interphalangeal joints only (“distal interphalangeal” pattern)
    • mutilating arthropathy (rare but severe)
    • spondylitis ± sacroiliitis
  • Workup if suspected:
    • X-rays: sacroiliac, hands (front/side), feet (front/side), spine
    • Ultrasound and MRI can be added
    • Acute phase reactants: ESR and PC (as spoken)
• Neoplasms (cancer risk):
  • Prevalence ~5%
  • Risk increases with longer psoriasis duration
  • Non-melanoma skin cancers: basal cell carcinoma, squamous cell carcinoma
  • Cutaneous T-cell lymphoma (CTCL) mentioned
  • Also cancers described in: urologic, respiratory, digestive tracts
  • Mechanism mentioned:
    • oxidative stress + cellular DNA damage
    • chronic immunosuppression from immunosuppressive therapy
    • toxic habits
• Mood disorders:
  • Higher risk of depression and anxiety, possible suicidal thoughts
  • Increased toxic habits (smoking/alcohol/drugs)
  • Quality-of-life disruption may be disproportionate to skin severity (face/genitals/visible areas)

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Treatment Methodology and Instruction-Style Guidance

1) Treatment Goals

• Control clinical manifestations
• Improve quality of life (aim to improve DLQI)
• Use the least harmful regimen possible
• “Target control” thresholds (as stated):
  • PASI < 3
  • Low quality-of-life index between 0 and 1
  • “Practically psoriasis does not affect quality of life”
• Response assessment:
  • An “answer” of 90 mentioned as evaluation of treatment working (exact label unclear)

2) General Measures (Lifestyle and Comorbidity Management)

• Lifestyle changes:
  • Physical activity
  • Stop toxic habits
  • Balanced diet
  • Weight loss (when applicable)
• Control comorbidities
  • Coordinate with attending physicians/cardiologists
• Psychotherapy
  • If necessary
• Patient education
  • Psoriasis is chronic
  • Treatments may be long-term
  • Disease may not be “cured,” but can be controlled
• Skin care / supportive management
  • Moisturize / emollients
  • Short baths, lukewarm water
  • Avoid excessive soap; use creamy soaps

3) Avoid Key Harm: Systemic Corticosteroids

Avoid inappropriate systemic corticosteroids because they may trigger/severe erythrodermic psoriasis after stopping.

4) Topical Treatments (Mild Psoriasis / Limited BSA)

• General use case: typically intended when impact < 5%
• Topical corticosteroids
  • Select potency based on:
    • plaque severity (erythema/scaling)
    • location:
      • face/folds → low potency
      • other areas → high potency
    • may combine with keratolytics (e.g., salicylic acid)
  • Safety cautions:
    • avoid excessive use
    • “rule of thumb”: ointment amount/usage should not be exceeded in 10 days (as stated)
• Vitamin D analogues
  • Example: calcipotriol
  • Can be used alone or with corticosteroids
  • Goal: minimize corticosteroid use
  • Mechanism noted: reduce pro-inflammatory cytokines
• Phototherapy
  • Narrowband UVB commonly mentioned
  • Can also be combined with psoralens (soralenes)
  • Indications:
    • larger body surface area involvement
    • adjunct to topical or systemic therapies
  • Advantage: can be used in children and pregnant women (as stated)
• Heliotherapy (controlled sunlight)
  • Anti-inflammatory/immunomodulatory effect
  • Exposure guidance (as described):
    • typically about one month
    • sunlight before 10 AM or after 4 PM
    • about 20 minutes on each side
  • Avoid sunburn and extensive exposure
  • Risk mitigation:
    • prevent Koebner/Köbner phenomenon (trauma-triggered lesions)

5) Systemic Treatments (When to Escalate)

Systemic therapy is indicated when:

• Moderate-to-severe psoriasis
• Joint involvement (psoriatic arthropathy)
• Disabling locations (hands/soles interfering with work/disability)
• Lack of adherence to topical therapy
• Practical limitation:
  • phototherapy often requires about twice weekly sessions; travel/distance may prevent use

6) Conventional Systemic Drugs (Monitoring and Key Constraints)

• Methotrexate
  • Common, accessible, affordable, good response
  • Antimetabolite/folate antagonist
  • Administration: oral (also intramuscular or subcutaneous)
  • Dose: maximum 25 mg/week
  • Folic acid regimen separation (example given: “2-day 5 mg folic acid”)
  • Risks/monitoring:
    • myelosuppression/pancytopenia (especially early)
    • labs within 15 days after starting; plus initial labs
    • possible hepatotoxicity; less frequently nephrotoxicity
  • Contraindications mentioned (not enumerated in subtitles)
  • Contraindicated in pregnancy and breastfeeding
• Acitretin
  • Systemic retinoid
  • Effective particularly for palmoplantar and pustular variants
  • Contraindications: pregnancy; requires strict contraception
  • Pregnancy washout rule: wait 2 years after stopping before trying to conceive
  • Monitoring:
    • liver function tests
    • lipid profile (may increase cholesterol/triglycerides)
• Cyclosporine
  • Used for erythrodermic or severe psoriasis needing a rapid response
  • Mechanistic notes (as spoken): blocks certain cytokine pathways (IL-12) and affects T-cell activation (e.g., CD4)