Page created on May 7, 2019. Last updated on May 4, 2020 at 19:25
Urticaria (commonly known as “hives”) is a condition where erythematous, oedematous and pruritic plaques called wheals arise on the skin. It can be caused by a multitude of factors, like allergens, insect bites, cold, stress, pressure and even normal water.
Pathogenesis: A type I hypersensitivity reaction against antigens like pollen, food or drugs causes mast cells in the skin to degranulate. This causes the small arteries in the dermis to become hyperpermeable, causing local oedema.
Urticaria caused by other factors don’t involve a type I hypersensitivity. The pathogenesis of these cases is unknown.
Treatment: Symptomatic cases can be treated with antihistamines or glucocorticoids.
Eczema describes any lesion of the skin that is pruritic (itchy), oedematous, erythematous (red) and oozing. There are multiple subtypes. We’ll look at two of them:
Atopic dermatitis is a poorly understood condition, but it has a strong genetic component. It often develops in people who also suffer from other atopic diseases like asthma and allergic rhinitis. It often involves the face and flexor surfaces. It’s a type I hypersensitivity reaction.
Contact dermatitis arises upon exposure to allergens. It’s a type IV hypersensitivity. It’s associated with:
- Poison ivy
- Chemicals like soap or perfume
- Certain drugs
Removing the offending irritant is often enough to cure contact dermatitis.
Psoriasis is a chronic dermatosis that affects 1 – 2% of the population. It is characterised by salmon-coloured plaques with silvery scales. It often affects the extensor surfaces of the knees and elbows and the scalp.
If one peels away the silvery scales small punctuate bleedings will occur under the scale. This is called Auspitz sign and can be used to diagnose psoriasis.
Pathogenesis: The etiology is unknown. A T-cell mediated immune response is involved. Affected people have some genetic predisposition and are exposed to some trigger factors like mechanical irritation or infection.
There is increased proliferation of keratinocytes. There is acanthosis and parakeratosis. Acanthosis refers to thickening of the epidermis while parakeratosis means that the keratinocytes in the stratum corneum have retained their nuclei.
Treatment: Topical corticosteroids are used first. In severe cases a treatment called PUVA (psoralen + UVA) can be used. It involves giving the patient a drug called psoralen, which makes the keratinocytes more susceptible to UV mediated-damage. UVA light is then applied to the lesion, which kills the hyperproliferative keratinocytes.
Erythema multiforme is a rare and self-limited hypersensitivity reaction to certain infections and drugs.
Morphology: Erythema multiforme gets the “multiforme” name from the fact that the lesions produced can take on a variety of forms. They usually start as erythematous macules, but they can progress into papules, vesicles and bullae. Lesions that look like targets are typical. These lesions have three rings, one inner red, one white and one outer red ring.
Pathogenesis: A hypersensitivity reaction against certain infections and drugs are the cause. The most common cause is HSV infection, which accounts for 50% of cases. Drugs like barbiturates, NSAIDs and penicillins are also frequent causes.
Complications: Two more severe forms of erythema multiforme are called toxic epidermal necrolysis (more severe) and Stevens-Johnson syndrome (less severe). These are often adverse drug reactions. In these conditions there is necrosis of the epidermis, which can be life-threatening.
Treatment: The condition is usually self-limiting, making treatment unnecessary.
Lichen planus is a chronic inflammatory disease. The cause is unknown. Its morphology is described as the five P’s:
- Pruritic (itchy)
- Planar (flat)
- Polygonal in shape
- Papules which are raised
The papules have characteristic white lines on them called Wickham striae. It often affects the wrists, elbows and oral mucosa. It can also occur on the genitals.
It’s caused by an immune response against the dermo-epidermal junction. Due to the bandlike infiltrate of lymphocytes along the dermoepidermal junction the rede ridges assume an angulated zigzag contour called sawtoothing. Anucleate necrotic basal cells are seen in the inflammed papillary dermis and are called either colloid bodies or Civatte bodies.
Lichen simplex chronicus
Lichen simplex chronicus is a thickening (lichenification) of the skin that occurs in response to local repetitive trauma to skin like continual rubbing or scratching. The trauma induces epithelial hyperplasia.
Morphology: The affected skin becomes thick, leathery and darkened. Histology shows acanthosis (thickened epidermis), hyperkeratosis (thickened stratum corneum) and hypergranulosis (thickened stratum granulosum).
Treatment: No treatment is needed.
The conditions listed below this point are blistering disorders of the skin. A blister occurs when layers of the skin separate. This can occur in two ways:
- The basal cells of the epidermis separate from the basement membrane they’re usually attached to. A big bubble-like space filled with fluid forms, which forms a blister.
- The different layers of the epidermis separate from each other, forming a blister.
Pemphigus vulgaris is an autoimmune disease where the immune system causes keratinocytes to separate from each other. This causes blisters to form. These blisters can affect both the oral mucosa and the skin.
Pathogenesis: The body produces IgG antibodies against the desmosomes that normally bind the keratinocytes of the epidermis together. As the desmosomes are destroyed the keratinocytes will separate from each other, forming a blister. The process where keratinocytes separate is called acantholysis.
Morphology: Blisters are formed inside the epidermis. The blisters can affect not only the skin but the oral mucosa as well. The blisters are thin and rupture easily.
Bullous pemphigoid is an autoimmune disease where the immune system causes basal cells to separate from the basal membrane. This causes blisters to form. These blisters affect most commonly the skin and rarely the oral mucosa.
Pathogenesis: The body produces IgG antibodies against the basement membrane of the epidermis. This destroys the hemidesmosomes that attach the basal cells to the basement membrane. The basal cells separate and form a blister.
Morphology: Blisters are formed below the epidermis. The blisters affect only the skin. These blisters are thicker and do not rupture easily. If immunofluorescence would be performed you would see antibodies lining up against the basement membrane, which forms a linear pattern.
Dermatitis herpetiformis is an autoimmune disease where the small vesicles develop at the tip of the dermal papillae. It most commonly occurs in people with coeliac disease.
Pathogenesis: IgA antibodies bind to proteins at the tips of dermal papillae. The resulting inflammation causes blisters to form. These IgA antibodies are the same that bind to gluten.
Morphology: Grouped small pruritic vesicles form on the skin. The vesicles are subepidermal. These vesicles are similar to those that develop in HSV infection, which gives the condition its name.