Psoriasis & Chronic Dermatitis
Psoriasis Verified · Sep 2026Psoriasis is a chronic immune-mediated disease in which activated T cells drive keratinocytes to multiply too quickly, forming scaly inflamed plaques; atopic dermatitis is a chronic itchy dermatitis built on a defective skin barrier; contact dermatitis is inflammation from direct chemical damage (irritant) or a delayed type IV hypersensitivity (allergic).
Why psoriasis plaques form and why the disease reaches the joints, heart and mood; the five psoriasis types and which two can be life-threatening; the atopic barrier defect and the atopic march; irritant versus type IV allergic contact dermatitis; and how to use topical steroids safely — thin skin, occlusion, children, and the label limits of a superpotent steroid such as clobetasol.
What’s going wrong in the body
The normal physiology, where it fails, and why the body’s compensation backfires.
01 Psoriasis — T cells tell skin cells to multiply too fast
Psoriasis is an immune disease that shows on the skin. "Psoriasis is a chronic (long-lasting) disease in which the immune system becomes overactive, causing skin cells to multiply too quickly. Patches of skin become scaly and inflamed, most often on the scalp, elbows, or knees, but other parts of the body can be affected as well." The mechanism: "The pathophysiology of psoriasis involves infiltration of the skin by activated T cells which stimulate the proliferation of keratinocytes. This dysregulation in keratinocyte turnover results in the formation of thick plaques." The scale has its own cause — "the epidermal cells fail to secrete lipids which results in flaky and scaly skin, which is typical of psoriasis." Epidermal hyperplasia is part of the picture (see the cellular adaptation page for the term).
Genes load it, the environment triggers it. "Scientists do not fully understand what causes psoriasis, but they know that it involves a mix of genetics and environmental factors," and "Many people with psoriasis have a family history of the disease." It runs in cycles: "The symptoms of psoriasis can sometimes go through cycles, flaring for a few weeks or months followed by periods when they subside or go into remission." There is no cure — "While there is currently no cure for psoriasis, there are treatments that keep symptoms under control" — and, the teaching point that matters most for body image, "Psoriasis is not contagious so you cannot catch it or spread it."
Injury to the skin makes new plaques. "Any injury to the skin in patients with psoriasis in the form of either mechanical, chemical, or radiational trauma induces lesions of psoriasis at that site which is called the Koebner phenomenon." Lift the scale off a plaque and the capillaries show: "On successive removal of psoriatic scales pinpoint bleeding points are seen. This is called the Auspitz sign." Certain drugs make it worse — "Certain drugs like chloroquine, lithium, beta-blockers, steroids, and NSAIDs can worsen psoriasis." — so every new prescription is a trigger check.
02 Five types of psoriasis — and the two that can be life-threatening
Plaque psoriasis is the common one. "This is the most common kind, and it appears as raised, red patches of skin that are covered by silvery-white scales. The patches usually develop in a symmetrical pattern on the body and tend to appear on the scalp, trunk, and limbs, especially the elbows and knees." It "affects 85% to 90% of patients." On brown or black skin, the NHS notes, patches can look "grey on brown or black skin, and cause dark marks on the skin after the psoriasis has gone." Nails pit and thicken — "Thick, ridged, pitted nails." Guttate "usually appears in children or young adults, and looks like small, red dots, typically on the torso or limbs. Outbreaks are often triggered by an upper respiratory tract infection, such as strep throat." Inverse "appears as smooth, red patches in folds of skin, such as beneath the breasts or in the groin or armpits. Rubbing and sweating can make it worse."
Pustular psoriasis — "pus-filled bumps called pustules surrounded by red skin appear. It usually affects the hands and feet, but there is a form that covers most of the body." The pustules are sterile: "Pustular psoriasis presents with small non-infectious pus-filled lesions with erythema surrounding it," and "Generalized pustular psoriasis is associated with hypocalcemia and presents with sterile pustules on an erythematous plaque involving the whole body."
Erythrodermic psoriasis "is a rare but severe form of psoriasis characterized by red, scaly skin over most of the body. It can be triggered by a bad sunburn or taking certain medications, such as corticosteroids." StatPearls names the classic trigger: "It is the result of an exacerbation of unstable plaque psoriasis, following the abrupt withdrawal of systemic steroids." The skin can no longer do its job: "Complications of erythroderma include impairment in barrier functions of the skin, disturbance in basal metabolic rate, and increased cutaneous circulation in turn affecting the heart with cardiac failure." The rule to remember: "Pustular psoriasis and erythrodermic psoriasis may be life-threatening." The NHS says to call 999 or go to A&E if "your skin quickly turns red and you develop white, pus-filled bumps that join together – redness may be harder to see on brown or black skin," especially with "other symptoms such as your heart beating fast, or a high temperature, or feeling hot, cold or shivery."
03 Psoriasis is a systemic disease — joints, heart, metabolism and mood
Psoriatic arthritis. "Psoriatic arthritis is a form of chronic inflammatory arthritis which affects 30% of patients with psoriasis." "It leads to sausage-shaped swelling of the fingers and toes known as dactylitis." NIAMS: "If you have symptoms of psoriatic arthritis, it is important to see your doctor soon because untreated psoriatic arthritis can lead to irreversible damage."
Heart and metabolism. NIAMS lists "Cardiovascular events, such heart attacks and strokes." and "People with psoriasis may also be more likely to get certain cancers, Crohn’s disease, diabetes, metabolic syndrome, obesity, osteoporosis, uveitis (inflammation of the middle of the eye), liver disease, and kidney disease." That is why "In the clinic, the patient should be screened for type 2 diabetes, hypertension, and dyslipidemia." Weight, smoking and alcohol all feed it: "Obesity makes the symptoms of psoriasis worse." "Studies have shown that the more a person smokes, the worse the symptoms tend to be." "Some studies suggest that excessive alcohol consumption aggravates symptoms."
Body image and mental health — the plan’s nursing focus. "The scaly patches of skin can make many people feel self-conscious about their appearance. Psoriasis can affect a person’s mental health, increasing the risk of anxiety and depression." Over time, "psoriasis has been associated with depression, suicide, alcoholism, smoking, substance abuse, metabolic syndrome, and a variety of skin cancers." And location matters: "patients with psoriasis involving the palms and soles tend to have a much poorer quality of life than those who have psoriasis on other parts of the body." The nursing action is explicit: "The nurse should monitor the patient for self-harm and refer the patient to a mental health counselor."
04 Atopic dermatitis — a leaky barrier and the itch–scratch cycle
Eczema is a barrier disease. "Atopic dermatitis, often referred to as eczema, is a chronic (long-lasting) disease that causes inflammation, redness, and irritation of the skin. It is a common condition that usually begins in childhood; however, anyone can get the disease at any age. Atopic dermatitis is not contagious, so it cannot be spread from person to person." The skin cannot hold water or keep things out: "Dysfunction of the epidermal barrier allows irritants and allergens to penetrate the epidermis and trigger inflammation through an exaggerated T-helper 2 (Th2) immune response." "Filaggrin mutations are present in up to 30% of patients with atopic dermatitis."
Itch drives damage, and damage drives itch. "New research suggests that inflammation directly triggers sensations of itch which in turn cause the patient to scratch. This leads to further damage of the skin as well as increased risk for infection with bacteria." Scratching "further aggravates inflammation by stimulating keratinocytes to release proinflammatory cytokines." The bacteria are already there: skin colonization by Staphylococcus aureus is common, "which occurs in more than 90% of patients," and "Colonization with S aureus can worsen inflammation and lead to secondary infection and impetiginization."
It is part of a family of allergic disease. "It is part of the atopic triad, which also includes allergic rhinitis and asthma. These conditions may develop concurrently or sequentially, in a progression known as the atopic march." It is common in children — "Atopic dermatitis affects approximately 10% to 30% of children and 2% to 10% of adults in developed countries" — and often fades: about 60% of cases start in the first year of life, "and about 60% resolving by age 12." Where it appears changes with age: infants on the face, scalp and around the joints (rarely the diaper area), children in the bends of the elbows and knees, neck and ankles, and "Adults typically present with chronic lichenified lesions with accentuated skin markings, often affecting the hands."
The complication that cannot wait. "A recognized complication of atopic dermatitis is Kaposi varicelliform eruption, which results from a primary herpes simplex virus infection." "Vesicular lesions typically arise within eczematous skin and may rapidly spread to unaffected areas. Prompt treatment with acyclovir can reduce morbidity." This is eczema herpeticum — clustered blisters in eczema that spread — and it is reported promptly.
05 Contact dermatitis — irritant damage versus type IV allergy
Two mechanisms, one look. "Irritant contact dermatitis is a nonspecific response of the skin to direct chemical damage that releases mediators of inflammation predominantly from epidermal cells while allergic contact dermatitis is a delayed (type 4) hypersensitivity reaction to exogenous contact antigens." Allergic contact dermatitis needs a prior exposure: "It is T-cell mediated inflammation of the skin caused by repeated skin exposure to haptens in a sensitized individual. Allergic contact dermatitis has two phases." — sensitization, then elicitation.
Timing tells them apart. "The acute irritant reaction usually reaches its peak quickly, within minutes to few hours after exposure." Allergic lesions come later: "Lesions usually appear 24 to 72 hours after the exposure to the causative agent and reach their peak at approximately 72 to 96 hours." The usual culprits: "Poison Ivy (Toxicodendron, formerly known as Rhus), in the United States, is considered to be the most common cause of allergic contact dermatitis." "Nickel is the most common metal present in artificial jewelry which is the cause of allergic contact dermatitis." And topical antibiotics can be the problem: "Neomycin and bacitracin applied to the areas of stasis dermatitis and leg ulcers may be the cause of allergic contact dermatitis on the legs and feet."
This is an occupational disease for nurses. "It is reported that up to 80% of cases of occupational dermatitis are irritant contact dermatitis," and the sourced example is "hand soap causing irritant dermatitis in a hospital employee." "In healthcare, latex allergy is a very common form of contact dermatitis and can have an impact on clinical practice." One variant is dangerous: contact urticaria, a wheal-and-flare reaction after exposure to the offending topical agent — "While most cases are mild, anaphylactic reactions can occur."
06 Topical corticosteroids — the shared tool, and its limits
How they work. "The mechanism of action of topical corticosteroids is extensive, involving anti-inflammatory, anti-mitotic, and immunosuppressive properties." "The anti-mitotic effect of topical corticosteroids plays a major role in psoriasis" — slowing the cell turnover that builds plaques. Potency runs across seven US classes, "class I superpotent and class VII least potent."
Where you put it changes how much gets in. "Corticosteroids are better absorbed and more permeable in regions of the thin epidermis, such as the eyelid, than thicker regions of the epidermis, such as the sole. The penetration difference between them varies by 300-fold." Inflamed skin absorbs more — "The penetration increases 2- to 10-fold in diseased states, such as inflammation and desquamation." — and "The application of occlusive dressings significantly enhances absorption." So "Low-to-medium strength preparations should be used for large surface areas to decrease the risk of systemic absorption," and "As a general rule, high-potency corticosteroids should not be used on thin skin, e.g. face, genitals, intertriginous areas, to avoid the risk of skin atrophy."
Local harm. "The most common local effects include atrophy, striae, rosacea, perioral dermatitis, acne, and purpura." "Areas most at risk for atrophy are intertriginous due to thinner skin and increased occlusion." Keep both halves of the atrophy fact: "Atrophy is reversible with cessation of steroid use; however, it may take months for the skin to appear normal again." but "Striae appear histologically as scars and are permanent." Steroids also hide infection: "Topical corticosteroids are contraindicated for bacterial infections as their anti-inflammatory and vasoconstrictive effect will mask the infection, ultimately delaying diagnosis and treatment." More is not better — in atopic dermatitis there is "no beneficial evidence for applying topical corticosteroids more than once daily. Applying it more often only increased adverse effects."
Systemic harm — and children absorb the most. "The systemic adverse effects include glaucoma, hypothalamic-pituitary axis suppression, Cushing syndrome, hypertension, and hyperglycemia." The label: "Systemic absorption of topical corticosteroids can produce reversible HPA axis suppression with the potential for glucocorticosteroid insufficiency after withdrawal from treatment." Children are at greater risk "Because of a higher ratio of skin surface area to body mass," and "HPA axis suppression, Cushing's syndrome, linear growth retardation, delayed weight gain and intracranial hypertension have been reported in children receiving topical corticosteroids." In an infant, "Manifestations of intracranial hypertension include bulging fontanelles, headaches, and bilateral papilledema."
The superpotent limits belong to the product label. For a superpotent steroid such as clobetasol propionate (FDA label): "Treatment beyond 2 consecutive weeks is not recommended"; "Use in pediatric patients under 12 years of age is not recommended."; "Clobetasol propionate gel, cream and ointment should not be used with occlusive dressings."; and it "should not be used on the face, groin, or axillae." When the skin clears, "therapy should be discontinued when control has been achieved." These are the clobetasol label’s rules — check the label of whatever product is ordered rather than applying them to every topical steroid.
Causes & risk factors
Modifiable factors are teaching targets — the patient can act on them.
Signs & symptoms
Each finding tied to the mechanism that produces it — and the triage it calls for.
Diagnostics
Complications
Medications for this condition
Why each class is prescribed here — every card links to its full pharmacology page.
The shared anti-inflammatory for all three diseases — anti-mitotic in psoriasis, and in atopic dermatitis "first-line agents for the treatment of acute flares," applied before the emollient. Match potency to site: no high-potency steroid on the face, genitals or skin folds; low-to-medium strength for large areas. For a superpotent steroid such as clobetasol, the label limits apply (not beyond 2 consecutive weeks, not under 12, no occlusion, not on face, groin or axillae).
Moderate-to-severe psoriasis: methotrexate ("It suppresses the immune system and slows down cell growth and division"), biologics that "block specific immune molecules," and other immunosuppressants for severe cases; systemic pills for severe atopic dermatitis "require close monitoring." Screen for TB and hepatitis before a biologic; monitor blood counts, liver and renal function.
Acyclovir for eczema herpeticum — "Prompt treatment with acyclovir can reduce morbidity."
Itch control in contact dermatitis — "Antihistamines such as hydroxyzine and cetirizine are recommended to control pruritus."
Caution, not a psoriasis or eczema treatment. Abrupt withdrawal of systemic steroids can trigger erythrodermic psoriasis; oral steroids are not usually given for atopic dermatitis because it "can flare or rebound and be more severe than before." In severe contact dermatitis only, systemic steroids "should be tapered gradually to prevent recurrences."
Beyond medications
- Moisturize — "Bathe in lukewarm water and use mild soap that has added oils. After bathing, apply heavy moisturizers while your skin is still damp." In atopic dermatitis, emollients twice daily, ideally within 3 minutes of a lukewarm shower or bath; ointments sting less than creams or lotions.
- Phototherapy for psoriasis — "Phototherapy is usually used when large areas of the skin are affected by the disease." Natural sun only in moderation: "Limited sunlight can alleviate symptoms, but too much can make them worse, so consult your doctor for advice."
- Other psoriasis topicals — vitamin D-based medicines, retinoids, coal tar, anthralin and PDE4 inhibitors.
- Calcineurin inhibitors (tacrolimus, pimecrolimus) for eczema on the face and skin folds, where steroids thin the skin.
- Avoid the cause in contact dermatitis — "Compliance with avoidance is important"; wash off urushiol as soon as possible after poison-ivy exposure.
- Bleach baths in atopic dermatitis only on the prescriber’s instructions — evidence is mixed.
- Lifestyle in psoriasis — healthy weight, a Mediterranean-style diet, quitting smoking, limiting alcohol, and a support group or mental-health provider.
Nursing considerations
The RN-specific layer — each action paired with the reason it matters.
How a real nurse thinks
The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.
- 1 Recognize cues
Red, scaly skin over most of the body with fever, chills and tachycardia — erythroderma with systemic signs.
Recent systemic steroid course that stopped three days ago; propranolol started two months ago; plastic-film occlusion over clobetasol; new plaques along a scratch; hopeless statements.
- 2 Analyze cues
Erythrodermic psoriasis "is the result of an exacerbation of unstable plaque psoriasis, following the abrupt withdrawal of systemic steroids"; beta-blockers also worsen psoriasis. The skin has lost its barrier and the extra skin circulation strains the heart.
Occlusion "significantly enhances absorption" and the clobetasol label forbids occlusive dressings. The new plaques along the scratch are the Koebner phenomenon.
"What’s the point" in someone isolated by a visible disease is a mood cue — psoriasis is associated with depression and suicide.
- 3 Prioritize
First: erythroderma with fever and tachycardia — "may be life-threatening." Then the self-harm cue, which needs a direct question before the shift moves on. Then the steroid and trigger teaching.
- 4 Generate solutions
Escalate the erythroderma now. Stop the plastic-film wrapping and report the occlusion use. Flag propranolol and the steroid course as psoriasis triggers for the prescriber. Ask directly about self-harm and arrange a mental-health referral.
- 5 Take action
SBAR: “42-year-old with long-standing plaque psoriasis, now red and scaly over most of the body for 2 days, T 38.4, HR 118, BP 108/64. Finished an oral prednisone course 3 days ago and takes propranolol. I am concerned about erythrodermic psoriasis and need you to see the patient now.”
Teach that psoriasis is not contagious, and that the ointment must not be wrapped.
- 6 Evaluate
Recheck temperature, heart rate and blood pressure after the escalation; confirm the wrapping has stopped; confirm the self-harm screen and referral are documented.
Scenario — you’re the nurse
Work each question before revealing the answer. Rationales explain the wrong options too.
42-year-old with plaque psoriasis for 20 years, uses clobetasol ointment. Two months ago started propranolol for migraine. Ten days ago an urgent-care clinic gave a short course of oral prednisone for bronchitis; the last dose was 3 days ago. Smokes a pack a day.
Q1 Multiple choice Which finding needs the most urgent action? - A. New plaques along a forearm scratch
- B. Red, scaly skin over most of the body with T 38.4 °C and HR 118
- C. A 20-year history of plaque psoriasis
- D. Using clobetasol ointment
Reveal answer & rationale
Q2 Select all that apply Which factors in this history can trigger or worsen psoriasis? Select all that apply. - A. Stopping oral prednisone
- B. Propranolol
- C. Smoking a pack a day
- D. Bathing in lukewarm water with oil-added soap
- E. The scratch on the forearm
Reveal answer & rationale
Q3 Multiple choice The patient wraps the clobetasol-treated legs in plastic film overnight. What is the best response? - A. “That is fine as long as you remove it in the morning.”
- B. “Wrapping makes more of the steroid get into your body, and this ointment should not be covered — please stop.”
- C. “Apply it three times a day instead of wrapping.”
- D. “Switch to wrapping only the elbows and knees.”
Reveal answer & rationale
Q4 Multiple choice The prescriber plans a biologic once the patient is stable. What should be done first? - A. Check the serum uric acid
- B. Screen for tuberculosis and hepatitis
- C. Give a smallpox vaccine
- D. Stop all moisturizers
Reveal answer & rationale
Q5 Multiple choice The patient says, “People move away from me on the bus. I don’t go out anymore. What’s the point.” What is the priority nursing response? - A. Reassure the patient that the rash will clear soon
- B. Ask directly about thoughts of self-harm and arrange a mental-health referral
- C. Change the subject to skin care
- D. Document the statement for the next shift
Reveal answer & rationale
Common questions
What causes psoriasis & chronic dermatitis?
Which findings should a nurse report immediately in psoriasis & chronic dermatitis?
Is psoriasis contagious?
Why can stopping steroid tablets make psoriasis worse?
Why shouldn’t you cover a steroid cream with a dressing?
What is the difference between irritant and allergic contact dermatitis?
Sources
- Psoriasis — StatPearls — StatPearls (NCBI Bookshelf)
- Atopic Dermatitis — StatPearls — StatPearls (NCBI Bookshelf)
- Contact Dermatitis — StatPearls — StatPearls (NCBI Bookshelf)
- Topical Corticosteroids — StatPearls — StatPearls (NCBI Bookshelf)
- Psoriasis — NHS. Contains public sector information licensed under the Open Government Licence v3.0 (https://www.nationalarchives.gov.uk/doc/open-government-licence/version/3/) — NHS (UK)
- Psoriasis: Overview, Symptoms, & Causes — NIAMS — NIAMS (NIH)
- Psoriasis: Diagnosis, Treatment, and Steps to Take — NIAMS — NIAMS (NIH)
- Atopic Dermatitis: Overview, Symptoms, & Causes — NIAMS — NIAMS (NIH)
- Atopic Dermatitis: Diagnosis, Treatment, and Steps to Take — NIAMS — NIAMS (NIH)
- Clobetasol propionate gel, cream and ointment 0.05% — FDA label (DailyMed) — FDA / DailyMed
Reviewed by Hae Suk Lee, RN
Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.