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Summary Table

Domain	Details
Risk Factors	Family history (strong genetic component, HLA-Cw6), obesity, smoking, alcohol use, stress, HIV/immunosuppression, streptococcal pharyngitis (guttate subtype)
Etiology	T-cell mediated autoimmune disease driven by Th1/Th17 pathway; aberrant keratinocyte proliferation with a turnover cycle shortened from ~28 days to 3 to 5 days
Patient Presentation	Chronic, relapsing, well-demarcated erythematous plaques with silvery-white scale; commonly on extensor surfaces (elbows, knees), scalp, and lumbosacral area; often pruritic
Classic Physical Exam	Auspitz sign (pinpoint bleeding upon scale removal), Koebner phenomenon (lesions at sites of trauma), nail pitting, oil-drop sign, onycholysis
Key Diagnostic Results	Clinical diagnosis in most cases; biopsy shows parakeratosis, acanthosis with regular elongation of rete ridges, Munro microabscesses (neutrophils in stratum corneum), thinned suprapapillary plates, dilated tortuous capillaries in dermal papillae
Management	Mild: topical corticosteroids and vitamin D analogs (calcipotriol). Moderate-to-severe: narrowband UVB phototherapy, methotrexate, cyclosporine, acitretin, or biologics (TNF-alpha, IL-17, IL-23 inhibitors)
Keywords	"Silvery scale," "well-demarcated plaques on extensors," "Auspitz sign," "nail pitting," "Koebner phenomenon," "strep throat then rash" (guttate), "pencil-in-cup deformity" (psoriatic arthritis)

1. Pathophysiology

Psoriasis is a chronic, immune-mediated inflammatory disease with a strong genetic predisposition. The strongest genetic association is with HLA-Cw6, a class I MHC molecule. Having a first-degree relative with psoriasis raises risk substantially.

The central driver is dysregulation of the adaptive immune system, particularly the Th1 and Th17 lymphocyte pathways. Dendritic cells in the skin become activated by various triggers (infection, trauma, stress, drugs such as lithium or beta-blockers) and migrate to regional lymph nodes, where they present antigens to naive T cells. This activates T cells that produce a cascade of pro-inflammatory cytokines: TNF-alpha, IL-17, IL-22, and IL-23. These cytokines act on keratinocytes and stimulate them to proliferate at a dramatically accelerated rate.

In normal skin, the keratinocyte turnover cycle takes approximately 28 to 30 days. In psoriatic skin, this is compressed to roughly 3 to 5 days. The keratinocytes do not have time to mature properly, which produces the characteristic parakeratosis (retention of nuclei in the stratum corneum). The silvery-white scale seen clinically is the gross manifestation of this thick, immature keratinized layer.

The inflammatory infiltrate also causes dilation of dermal capillaries and neovascularization in the dermal papillae. These dilated, tortuous vessels sit very close to the surface because the suprapapillary plate (the epidermis overlying the papillae) is thinned. This explains the Auspitz sign: when you peel off the adherent silvery scale, you expose these superficial capillaries and trigger pinpoint bleeding.

Munro microabscesses, collections of neutrophils within the parakeratotic stratum corneum, are the hallmark histological finding. Neutrophils are recruited by IL-8 and other chemokines released by activated keratinocytes.

The Koebner phenomenon (isomorphic response) occurs because the immune priming in psoriasis is systemic, not localized. Any trauma to the skin recruits immune cells and cytokines to the site of injury, triggering a new psoriatic plaque at that location. This is why vignettes may describe lesions appearing at a surgical scar or site of a scratch.

2. Classification and Clinical Manifestation

Subtype	Frequency	Clinical Features	Key Associations
Plaque (Vulgaris)	~80 to 90% of cases	Well-demarcated, raised, erythematous plaques with thick silvery-white scale on extensor surfaces, scalp, lumbosacral region	Most common subtype; chronic relapsing course
Guttate	~10%	Multiple small (< 1 cm), drop-shaped, salmon-pink papules with fine scale; widespread, trunk predominant	Triggered by Group A Streptococcal pharyngitis 2 to 3 weeks prior; more common in children and young adults; may resolve spontaneously
Inverse (Flexural)	Uncommon	Smooth, shiny, erythematous patches in intertriginous areas (axillae, groin, inframammary folds); minimal scale due to moisture	Often confused with fungal intertrigo or candidiasis; KOH prep negative
Pustular (Generalized / von Zumbusch)	Rare	Widespread sterile pustules on erythematous base; fever, leukocytosis, systemic toxicity	Medical emergency; can be triggered by abrupt withdrawal of systemic corticosteroids; cultures are sterile
Pustular (Localized / Palmoplantar)	Uncommon	Sterile pustules confined to palms and soles	Chronic, debilitating; associated with smoking
Erythrodermic	Rare	Generalized erythema and scale involving >90% of body surface area; systemic symptoms (fever, hypothermia, tachycardia)	Life-threatening; risk of high-output cardiac failure, sepsis, electrolyte imbalance, thermoregulatory failure
Nail Psoriasis	50% of plaque patients	Nail pitting, oil-drop discoloration, onycholysis, subungual hyperkeratosis	Strongly associated with psoriatic arthritis
Psoriatic Arthritis	~30% of psoriasis patients	Asymmetric oligoarthritis or polyarthritis; DIP joint involvement, dactylitis ("sausage digits"), enthesitis	RF-negative, anti-CCP negative; X-ray shows "pencil-in-cup" deformity and periostitis

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination	Best initial approach; sufficient for most cases	Well-demarcated plaques with silvery scale on extensor surfaces; Auspitz sign; Koebner phenomenon
Skin biopsy	Confirmatory test when diagnosis is uncertain	Parakeratosis, regular acanthosis, elongated rete ridges, Munro microabscesses, dilated capillaries in dermal papillae, thinned suprapapillary plates
KOH preparation	To exclude tinea	Negative (rules out dermatophyte infection)
ASO titer / Throat culture	When guttate psoriasis is suspected	Evidence of recent streptococcal infection
Rheumatoid factor (RF) and Anti-CCP	When psoriatic arthritis is considered	Both negative (seronegative spondyloarthropathy)
X-ray of affected joints	Psoriatic arthritis evaluation	Pencil-in-cup deformity, periostitis, joint space narrowing, ankylosis in advanced disease
ESR / CRP	Non-specific inflammation markers	Elevated in active psoriatic arthritis or erythrodermic/pustular variants
Metabolic screening	Comorbidity assessment	Lipid panel, fasting glucose, HbA1c (strong association with metabolic syndrome)

Psoriasis is overwhelmingly a clinical diagnosis. The combination of well-demarcated erythematous plaques with adherent silvery scale on extensor surfaces, positive Auspitz sign, and the classic distribution pattern (elbows, knees, scalp, lumbosacral region, nails) is usually sufficient.

A skin biopsy becomes necessary when the presentation is atypical, when you need to differentiate from mimics such as cutaneous T-cell lymphoma (mycosis fungoides), or when the patient fails initial therapy. The histological pattern is highly characteristic: regular acanthosis with elongation of rete ridges (sometimes described as a "test-tube" pattern), thinning of the suprapapillary plate, parakeratosis, and Munro microabscesses. These findings together are essentially pathognomonic.

For guttate psoriasis, always consider checking an ASO titer or obtaining a throat culture. The classic vignette describes a child or adolescent who develops a widespread, droplet-like rash 2 to 3 weeks after a sore throat. Confirming recent streptococcal infection supports the diagnosis and may guide treatment with antibiotics if the infection is still active.

When psoriatic arthritis is on the differential, the key lab finding is seronegativity for RF and anti-CCP. This distinguishes it from rheumatoid arthritis. Imaging reveals characteristic changes at the DIP joints, including the pencil-in-cup deformity, periostitis, and new bone formation. The pattern of joint involvement (DIP predominance, dactylitis, enthesitis, asymmetry) further distinguishes it from RA.

Do not forget comorbidity screening. Psoriasis carries elevated risk for cardiovascular disease, metabolic syndrome, non-alcoholic fatty liver disease, and depression. Vignettes may test your awareness of these associations.

4. Management and Treatment

Severity	First-Line Therapy	Alternatives / Adjuncts
Mild (< 5% BSA)	Topical high-potency corticosteroids (betamethasone dipropionate 0.05% ointment, applied once to twice daily) + topical vitamin D analog (calcipotriol 0.005%)	Topical retinoid (tazarotene), coal tar preparations, topical calcineurin inhibitors (tacrolimus/pimecrolimus for face and flexures)
Moderate (5 to 10% BSA)	Combination calcipotriol/betamethasone dipropionate ointment; if insufficient, add narrowband UVB phototherapy	PUVA (psoralen + UVA) for refractory cases
Severe (> 10% BSA or refractory)	Narrowband UVB phototherapy or systemic therapy: methotrexate, cyclosporine, acitretin	Biologic agents: adalimumab, secukinumab, ustekinumab, guselkumab; PDE4 inhibitor (apremilast)
Pustular / Erythrodermic	Hospitalization, systemic therapy (cyclosporine for rapid control or acitretin), biologics	Supportive care: fluid resuscitation, temperature management, infection prevention
Psoriatic Arthritis	NSAIDs for mild disease; methotrexate for moderate joint disease; TNF-alpha inhibitors (adalimumab) or IL-17 inhibitors (secukinumab) for moderate-to-severe	Apremilast, ustekinumab

Mild disease is treated with topical agents. The backbone of topical therapy is corticosteroids. For body and extremity plaques, use medium-to-high potency steroids (e.g., betamethasone dipropionate 0.05%, clobetasol propionate 0.05%) applied once to twice daily for 2 to 4 weeks, then taper. For the face, genitals, and intertriginous areas, use low-potency steroids (hydrocortisone 1%) or preferably topical calcineurin inhibitors (tacrolimus 0.1% ointment) to avoid steroid-induced skin atrophy in thin-skinned areas.

Vitamin D analogs (calcipotriol/calcipotriene 0.005%) are frequently combined with topical steroids. They work by inhibiting keratinocyte proliferation and promoting differentiation. The combination product (calcipotriol + betamethasone dipropionate) is superior to either agent alone and is a commonly tested first-line choice.

When topical therapy is inadequate, the next step is phototherapy. Narrowband UVB (NB-UVB) is the preferred modality, typically administered 3 times per week for 12 to 24 weeks. It works by inducing T-cell apoptosis in the skin. PUVA (oral psoralen plus UVA light) is reserved for refractory cases because of its higher long-term risk of squamous cell carcinoma and cataracts.

Systemic therapy is indicated for moderate-to-severe disease or when phototherapy is impractical.

Methotrexate is often the first-line systemic agent. It is given at 7.5 to 25 mg orally or subcutaneously once weekly, supplemented with folic acid 1 mg daily (except on the methotrexate day) to reduce mucosal and hematologic side effects. Monitoring requires a baseline CBC, liver function tests (LFTs), and renal function, repeated every 1 to 3 months. The major long-term concern is hepatotoxicity and hepatic fibrosis. Methotrexate is absolutely contraindicated in pregnancy (FDA Category X; teratogenic) and in patients with significant liver disease or active infection.

Cyclosporine (3 to 5 mg/kg/day divided twice daily) provides rapid disease control and is useful for acute flares or as a bridge to slower-acting therapies. Its use is limited to 1 to 2 years due to the risk of nephrotoxicity and hypertension. Monitor blood pressure, serum creatinine, and potassium regularly.

Acitretin (25 to 50 mg daily) is an oral retinoid particularly useful for pustular and erythrodermic psoriasis. It is teratogenic with an exceptionally long washout period: women must avoid pregnancy for 3 years after discontinuation (because acitretin can be converted to etretinate in the presence of alcohol, and etretinate has a half-life of 120 days stored in adipose tissue).

Biologic agents represent the most targeted therapies and are reserved for moderate-to-severe disease failing conventional systemic treatment.

TNF-alpha inhibitors: adalimumab (40 mg subcutaneously every 2 weeks), etanercept, infliximab. Screen for latent tuberculosis (PPD or interferon-gamma release assay) and hepatitis B before initiation.
IL-17 inhibitors: secukinumab (300 mg subcutaneously, loading dose at weeks 0, 1, 2, 3, 4, then monthly), ixekizumab.
IL-12/23 inhibitor: ustekinumab (45 mg for patients under 100 kg, 90 mg for patients over 100 kg, subcutaneously at weeks 0, 4, then every 12 weeks).
IL-23 inhibitors: guselkumab, risankizumab (among the most effective agents, with dosing every 8 to 12 weeks after loading).

Apremilast (30 mg orally twice daily after a titration week) is a PDE4 inhibitor that offers oral convenience without immunosuppression-level monitoring but has modest efficacy compared to biologics.

Critical contraindications to remember: Never abruptly withdraw systemic corticosteroids in a psoriasis patient, as this can precipitate a pustular or erythrodermic flare. This is a classic exam trap.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Seborrheic Dermatitis	Scaly, erythematous patches on the scalp; can overlap with psoriasis ("sebopsoriasis")	Seborrheic dermatitis has greasy, yellowish scale in seborrheic zones (nasolabial folds, eyebrows, post-auricular); psoriasis has dry, silvery-white scale and involves extensor surfaces
Atopic Dermatitis (Eczema)	Pruritic, chronic, relapsing skin condition	Eczema favors flexural surfaces (antecubital, popliteal fossa), has poorly defined borders, and is associated with atopy (asthma, allergic rhinitis); psoriasis favors extensors and has well-demarcated borders
Pityriasis Rosea	Widespread scaly papules/patches, especially in young adults	Begins with a herald patch followed by a "Christmas tree" distribution on the back; oval, salmon-colored with collarette scale; self-limited (6 to 8 weeks)
Tinea Corporis	Annular, scaly, erythematous plaques	Central clearing with an active, raised border; KOH prep shows hyphae; psoriasis has uniform thickness without central clearing
Lichen Planus	Purple, polygonal, pruritic papules; can affect skin and nails	Favors wrists, ankles, oral mucosa; Wickham striae (white lacy lines on mucosal lesions); histology shows band-like lymphocytic infiltrate at dermoepidermal junction, not Munro microabscesses
Secondary Syphilis	Widespread papulosquamous rash involving palms and soles	Non-pruritic, involves palms and soles (unusual for psoriasis except palmoplantar subtype); history of painless genital ulcer (chancre); positive RPR/VDRL and FTA-ABS
Mycosis Fungoides (Cutaneous T-cell Lymphoma)	Chronic, scaly patches/plaques; may mimic psoriasis clinically	Lesions progress from patches to plaques to tumors over years; bathing trunk distribution; biopsy shows atypical lymphocytes with cerebriform nuclei (Pautrier microabscesses), not Munro microabscesses
Nummular Eczema	Coin-shaped, scaly plaques	Lesions are intensely pruritic with vesicles and crusting; lack the thick silvery scale and well-demarcated borders of psoriasis; do not show Auspitz sign

6. Traps and High-Yield Pearls

The most common way students lose points on psoriasis questions is by confusing flexural and extensor predilection. Psoriasis favors extensors (elbows, knees); eczema favors flexors. When a vignette describes a well-demarcated, silvery-scaled plaque on the elbow of an adult, psoriasis is the answer. When it describes an ill-defined, oozing, excoriated patch in the antecubital fossa of a child with a history of asthma, it is eczema. This extensor-versus-flexor distinction is the single most tested discriminator.

The second major trap is the guttate psoriasis vignette. Test-writers will describe a teenager who presents with a sudden eruption of small, drop-like, scaly papules on the trunk 2 to 3 weeks after a sore throat. Students who do not link the preceding streptococcal pharyngitis to the rash will miss this diagnosis. Always look for a recent upper respiratory infection in a young patient with new-onset widespread small papules.

Third, be alert for the steroid withdrawal trap. A vignette may describe a psoriasis patient who was placed on systemic corticosteroids (perhaps for another condition) and then had them stopped abruptly, triggering a catastrophic pustular or erythrodermic flare. The core competency here is recognizing that systemic corticosteroids should never be used as long-term therapy for psoriasis and should never be withdrawn suddenly.

Fourth, remember the nail and joint connection. When a vignette describes nail pitting plus asymmetric DIP joint swelling with a negative RF, the answer is psoriatic arthritis. The seronegative arthritis pattern (RF-negative, anti-CCP-negative) with DIP involvement, dactylitis, or enthesitis points directly to psoriatic arthritis over rheumatoid arthritis. Pencil-in-cup deformity on X-ray seals the diagnosis.

Finally, do not overlook the comorbidity angle. A question may present a patient with known psoriasis and then ask about cardiovascular risk stratification or metabolic syndrome screening. Psoriasis is an independent risk factor for cardiovascular events, and this association is increasingly tested.

The core competency being assessed across psoriasis questions is your ability to recognize the classic clinical morphology (well-demarcated, silvery, extensor plaques), connect subtypes to their triggers (strep for guttate, steroid withdrawal for pustular/erythrodermic), sequence management correctly (topical before phototherapy before systemic before biologic), and identify the seronegative arthritis pattern when joints are involved.

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