Impetigo - A Brief Discussion.

Introduction: This is the most superficial of the bacterial skin infections. It is one of the most common skin infections in children. but can also occur in adults.

Etiology: It is caused by Streptococcus pyogenes or Staph. aureus infecting the epidermal layer of the skin.

Clinical features: Because it is so superficial, there is weeping, crusting, and oozing of the skin.
Symptoms start with red or pimple-like sores surrounded by red skin. These sores can be anywhere, but usually occur on the face, arms and legs. The sores fill with pus, then break open after a few days and form a thick crust. They are often itchy, but scratching them can spread the sores.

Impetigo is contagious and can be spread to others through close contact or by sharing towels, sheets, clothing, toys, or other items.

Diagnosis: A specific microbiologic diagnosis is rarely made or necessary. It is mostly diagnosed by the clinical appearance of  “weeping, oozing, honey-colored lesions.”

Introduction to Alopecia

Alopecia, or hair loss, usually occurs on the scalp; hair loss elsewhere on the body is less common and less conspicuous. In the nonscarring form of this disorder (noncicatricial alopecia), the hair follicle can generally regrow hair. But scarring alopecia usually destroys the hair follicle, making hair loss irreversible.

Causes
The most common form of nonscarring alopecia is male pattern alopecia, which appears to be related to androgen levels and to aging. Genetic predisposition commonly influences the time of onset, degree of baldness, speed with which it spreads, and pattern of hair loss. Women may experience a similar disorder, called androgenetic alopecia, characterized by diffuse thinning over the top of the scalp.

Other forms of nonscarring alopecia include:

• physiologic alopecia (usually temporary): sudden hair loss in infants, loss of straight hairline in adolescents, and diffuse hair loss after childbirth
• alopecia areata (an autoimmune disorder): generally reversible and self-limiting; usually occurs in young and middle-aged adults of both sexes; also occurs in children
• trichotillomania: compulsive pulling, plucking or twisting of one’s own hair; usually occurs in children.

Predisposing factors of nonscarring alopecia also include radiation, many types of drug therapies and drug reactions, bacterial and fungal infections, psoriasis, seborrheic dermatitis (from scratching the affected area), and endocrine disorders, such as thyroid, parathyroid, and pituitary dysfunctions.

Scarring alopecia causes irreversible hair loss. It may result from physical trauma, or chemical toxicity, or chronic tension or traction on a hair shaft, as occurs in braiding or using hot rollers or hot combs. Diseases that produce scarring alopecia include destructive skin tumors, granulomas, lupus erythematosus, scleroderma, follicular lichen planus, and severe fungal, bacterial, or viral infection, such as kerion, deep folliculitis, and herpes zoster.

Introduction to Scabies

An age-old skin infection, scabies results from infestation with Sarcoptes scabiei var. hominis (itch mite), which provokes a sensitivity reaction. It occurs worldwide, is predisposed by overcrowding and poor hygiene, and can be endemic.

Causes
Mites can live their entire life cycles in the skin of humans, causing chronic infection. The female mite burrows into the skin to lay her eggs, from which larvae emerge to copulate and then reburrow under the skin.
Transmission of scabies occurs through skin or sexual contact. The adult mite can survive without a human host for only 2 to 3 days.

Signs and symptoms
Typically, scabies causes itching that intensifies at night. Characteristic lesions take many forms but are usually excoriated and may appear as erythematous nodules.
Burrows are threadlike lesions about ¾? (2 cm) long and generally occur between fingers, on flexor surfaces of the wrists, on elbows, in axillary folds, at the waistline, on nipples in females, and on genitalia in males. In infants, the burrows may appear on the head and neck.
Intense scratching can lead to severe excoriation and secondary bacterial infection. Itching may become generalized secondary to sensitization.

Diagnosis
Superficial scraping and examination, under a low-power microscope, of material that has been expressed from a burrow may reveal the mite, ova, or mite feces. However, excoriation or inflammation of the burrow can make such identification difficult.
If diagnostic tests offer no positive identification of the mite and if scabies is still suspected (for example, close contacts of the patient also report itching), skin clearing that occurs after a therapeutic trial of a pediculicide confirms the diagnosis.

Urticaria And Angioedema

Urticaria, commonly known as hives, is an episodic, usually self-limited skin reaction characterized by local dermal wheals surrounded by an erythematous flare. 

Angioedema, which can present either subcutaneously or dermally, produces deeper, larger wheals (usually on the hands, feet, lips, genitals, and eyelids) and a more diffuse swelling of loose subcutaneous tissue. Urticaria and angioedema can occur simultaneously, but angioedema may last longer.

Pathophysiology
Urticaria and angioedema are common allergic reactions. Causes include allergy to drugs, foods, insect stings and, occasionally, inhalants, such as animal dander and cosmetics, that provoke an immunoglobulin (Ig) E-mediated response to protein allergens. However, certain drugs may cause urticaria without an IgE response.
When urticaria and angioedema are part of an anaphylactic reaction, they almost always persist long after the systemic response has subsided. This occurs because circulation to the skin is inhibited after an allergic reaction, which results in slow histamine reabsorption at the reaction site. Nonallergic urticaria and angioedema are probably also related to histamine release.
External physical stimuli, such as cold (usually in young adults), heat, water, or sunlight, may provoke urticaria and angioedema. Dermographism urticaria develops with varying pressure, usually under tight clothing, and is aggravated by scratching.
Several different mechanisms and underlying disorders may provoke urticaria and angioedema. These include IgE-induced release of mediators from cutaneous mast cells; binding of IgG or IgM, resulting in complement activation; localized or secondary infections such as respiratory infection; neoplastic diseases such as Hodgkin’s disease; connective tissue diseases such as systemic lupus erythematosus; collagen vascular diseases; and psychogenic diseases.

Signs and symptoms
The characteristic features of urticaria are distinct, raised, evanescent dermal wheals surrounded by an erythematous flare. These lesions may vary in size. In cholinergic urticaria, the wheals may be tiny and blanched, surrounded by erythematous flares.

Angioedema characteristically produces nonpitted swelling of deep subcutaneous tissue, usually on the eyelids, lips, genitalia, and mucous membranes. These swellings don’t usually itch but may burn and tingle.

Introduction to Atopic Dermatitis

Atopic dermatitis is characterized by superficial skin inflammation and intense itching. Although atopic dermatitis may appear at any age, it typically begins during infancy or early childhood. It may then subside spontaneously, followed by exacerbations in late childhood, adolescence, or early adulthood. Atopic dermatitis affects less than 1% of the population.

Causes
Atopic dermatitis is a chronic, inherited skin disorder in which the immune system produces a hypersensitivity reaction to environmental allergens that are often difficult to identify.

Exacerbating factors of atopic dermatitis include irritants, infections (commonly caused by Staphylococcus aureus), and some allergens. Although no reliable link exists between atopic dermatitis and exposure to inhalant allergens (such as house dust and animal dander), exposure to food allergens (such as soybeans, fish, or nuts) may coincide with flare-ups of atopic dermatitis.

Signs and symptoms
Scratching the skin causes vasoconstriction and intensifies pruritus, resulting in erythematous and weeping lesions. Eventually, the lesions become scaly and lichenous. Usually, they’re located in areas of flexion and extension, such as the neck, antecubital fossa, popliteal folds, and the backs of the ears. Patients with atopic dermatitis are prone to unusually severe viral infections, bacterial and fungal skin infections, ocular complications, and allergic contact dermatitis.

Introduction to Burns

A major burn is a horrifying injury, necessitating painful treatment and a long period of rehabilitation. It’s often fatal or permanently disfiguring and incapacitating (emotionally and physically). In the United States, about 2.5 million people annually suffer burns. It’s the nation’s third leading cause of accidental death.

Causes
Thermal burns, the most common type, are caused by flame, flash, scald or contact with hot objects. Examples are residential fires, motor vehicle accidents, playing with matches, improperly stored gasoline, space heater or electrical malfunctions, or arson. Other causes include improper handling of firecrackers, scalding accidents, and kitchen accidents (such as a child climbing on top of a stove or grabbing a hot iron). Burns in children are sometimes traced to parental abuse.
Chemical burns result from the contact, ingestion, inhalation, or injection of acids, alkalis, or vesicants that cause tissue injury and necrosis. 

Electrical burns result from coagulation necrosis caused by intense heat; they usually occur after contact with faulty electrical wiring or high-voltage power lines or when electric cords are chewed (by young children). Friction or abrasion burns happen when the skin is rubbed harshly against a coarse surface. 

Sunburn, of course, follows excessive exposure to sunlight.

Signs and symptoms
Symptoms will vary depending on the degree of burn. Suspect burn injury when the patient presents with blisters, pain, peeling skin, red skin, edema, white or charred skin, or signs of shock. Suspect an airway burn if you see charred mouth, burned lips, burns on the head, neck, or face; wheezing, change in voice, difficulty breathing and coughing; singed nose hairs or eyebrows; or dark carbon-stained mucous.

Pemphigus Vulgaris A Dermatological Condition

Introduction
Pemphigus is derived from the Greek word pemphix meaning bubble or blister.

The term pemphigus refers to a group of autoimmune blistering diseases of the skin and mucous membranes characterized histologically by intraepidermal blister and immunopathologically by the finding of in vivo bound and circulating immunoglobulin G (IgG) antibody directed against the cell surface of keratinocytes.

Pathophysiology
Pemphigus vulgaris is an autoimmune, intraepithelial, blistering disease affecting the skin and mucous membranes and is mediated by circulating autoantibodies directed against keratinocyte cell surfaces.

Blisters in pemphigus vulgaris are associated with the binding of IgG autoantibodies to keratinocyte cell surface molecules. These intercellular or pemphigus vulgaris antibodies bind to keratinocyte desmosomes and to desmosome-free areas of the keratinocyte cell membrane. The binding of autoantibodies results in a loss of cell-to-cell adhesion, a process termed acantholysis. The antibody alone is capable of causing blistering without complement or inflammatory cells.

Incidence
Pemphigus vulgaris has been reported to occur worldwide. Pemphigus vulgaris incidence varies from 0.5-3.2 cases per 100,000 population. Pemphigus vulgaris incidence is increased in patients of Ashkenazi Jewish descent and those of Mediterranean origin. Few familial cases have been reported.

The male-to-female ratio is approximately equal. In adolescence, girls are more likely to be affected than boys.

The mean age of onset is approximately 50-60 years.

Conditions Causing Skin Hyper pigmentation

Sometimes in medical practice patients presents with skin hyperpigmentation or pigmented spots. There are many underlying different causes and they are briefly discussed here:

1. Endocrine Disorders

• Addison’s disease
• Cushing’s syndrome
• Acromegaly
• Nelson’s syndrome
• Pregnancy
• Porphyria

2. Renal Failure

3. Cirrhosis

4. Haemochromatosis

5. Nutritional Causes:

• Vitamin B12 deficiency
• Pellagra

6.. Amyloid

7. Acanthosis nigricans

Acne Vulgaris - Brief Discussion

Introduction: Acne vulgaris is a common skin disorder which usually occurs in adolescence. It typically affects the face, neck and upper trunk and is characterised by the obstruction of the pilosebaceous follicle with keratin plugs which results in comedones, inflammation and pustules.

Epidemiology: affects around 80-90% of teenagers, 60% of whom seek medical advice. Acne may also persist beyond adolescence;

Etiology And Pathophysiology : is multifactorial

• Follicular epidermal hyperproliferation resulting in the formation of a keratin plug.
• This in turn causes obstruction of the pilosebaceous follicle. 
• Activity of sebaceous glands may be controlled by androgen, although levels are often normal in patients with acne
• Colonisation by the anaerobic bacterium Propionibacterium acnes
• Inflammation

Clinical Features: Acne is a disease of the pilosebaceous unit. 

Several different types of acne lesions are usually seen in each patient

Comedones are due to a dilated sebaceous follicle

• if the top is closed a whitehead is seen
• if the top opens a blackhead forms

Inflammatory lesions form when the follicle bursts releasing irritants

• papules
• pustules

An excessive inflammatory response may result in:

• nodules
• cysts

This sequence of events can ultimately cause scarring

• icepick scars
• hypertrophic scars

In contrast, drug nduced acne is often monomorphic (e.g. pustules are characteristically seen in steroid use)

Acne fulminans is very severe acne associated with systemic upset (e.g. fever). Hospital admission is often required and the condition usually responds to oral steroids.

Classification Of Acne Based On Severity Of Symptoms: Acne may be classified into:

1. Mild: open and closed comedones with or without sparse inflammatory lesions

2. Moderate acne: widespread noninflammatory lesions and numerous papules and pustules

3.Severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring.

Management: A simple management scheme often used in the treatment of acne is as follows:

• single topical therapy (topical retinoids, benzyl peroxide)
• topical combination therapy (topical antibiotic, benzoyl peroxide, topical retinoid)
• oral antibiotics: e.g. Oxytetracycline, doxycycline. Improvement may not be seen for 34 months. Minocycline is now considered less appropriate due to the possibility of irreversible pigmentation. Gram negative folliculitis may occur as a complication of longterm antibiotic use high dose - oral trimethoprim is effective if this occurs
• oral isotretinoin: only under specialist supervision
• There is no role for dietary modification in patients with acne.

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