Description and SymptomsFacial acne like pimples along with redness, telangiectases and flushing in adults. Usually asymptomatic, though eye involvement may be irritating. Key diagnostic feature is the lack of comedones.
Diagnosis Clinical.
Pathology Unknown cause, but higher predisposition in fair skinned female patients. Very common.
Principles of therapy Avoid triggers (stress, heat, alcohol).
Metronidazole gel or the
tetracycline class of antibiotics.
Description and SymptomsScaly, red plaques that tend to affect the knees, elbows, scalp and sacrum. Most patients have a few small asymptomatic plaques, however some have widespread lesions & /or pruritus. 1% incidence. Possible autosomal dominant inheritance with variable penetrance.
Diagnosis Clinical appearance, though may confirm with a biopsy.
Pathology An inflammatory reaction in the skin altered by environmental and genetic factors.
Principles of TherapyAggressiveness of therapy must be tailored to clinical situation. Many options available: topical (steroids, calcipotriene, retinoids), ultraviolet light (A&B), and systemic (
methotrexate, retinoids, cyclosporine, TNF-alpha inhibitors).
Description and SymptomsPhotodistributed blisters, crusts and erosions that lead to scars and pigmentary changes. May be associated with milia, hypertrichosis and sclerodermoid changes.
Diagnosis Clinical suspicion confirmed by urine or serum porphyrins.
PathologyMay be associated with viral hepatitis, hormonal therapies, hemodialysis or alcohol intake. Etiology is a defect in the uroporphyrinogen decarboxylase enzyme used in the production of heme.
Principles of TherapyComplete sun protection extremely important. Treatment of underlying disorder. Phlebotomy and low-dose antimalarials (
hydroxychloroquine) are treatment options.
Description and SymptomsTransient eruption that tends to occur on the trunk of young adults. The first sign is usually a large red scaly plaque (Herald patch), followed later by smaller oval scaly plaques. The eruption lasts 3-8 weeks.
Diagnosis Clinical, however may be mimicked by syphilis (check RPR).
Pathology Unknown etiology.
Principles of Therapy No therapy needed. If symptomatic, topical steroids or UV light may be helpful.
Description and SymptomsChronic eruption that affect the mucous membranes, skin and nails. The buccual mucosa often has a lacy white appearance. The skin has itchy reddish-purple flat topped papules with an overlying fine white lacy scale (Wickham’s striae) most commonly seen on the wrists, genitalia and ankles. The nails may be normal, but may be severely dystrophic.
Diagnosis Clinical suspicion confirmed by biopsy.
PathologyUnknown. Some drug eruptions can mimic rash. In addition, some studies indicate an association between L.P. and Hepatitis C.
Principles of Therapy Topical steroids [
Clobetasol (strong), Triamcinolone (mod.), Hydrocortisone (mild)] and antihistamines. Drug history and Hepatitis screen may be helpful.
Description and SymptomsPurpuric papules most often on the lower extremities usually lasting several weeks. Commonly associated with fever, arthralgias and other systemic symptoms including renal involvement. May be idiopathic or associated with a variety of triggering factors (medications, infections, connective tissue disorders).
Diagnosis Clinical suspicion confirmed by biopsy.
Pathology Immune complex deposition in the cutaneous vessels leading to vascular destruction and extravasation of RBC’s.
Principles of Therapy If possible, treatment of the precipitating event or disorder. A variety of medications can be helpful:
NSAIDS, Dapsone, Colchicine or Prednisone.
Description and SymptomsBrown well demarcated macules in areas of chronic sun damage (often the face, neck, upper chest, forearms and hands). Commonly referred to as “liver spots” or “age spots”.
Diagnosis Clinical. Biopsy is occasionally needed to exclude skin cancer.
Pathology Increased pigmentation & number of melanocytes in the epidermis. Unlike nevi, no nests are seen.
Principles of Therapy No treatment needed unless for cosmetic purposes. Laser or LN2 may be used.
Description and SymptomsRed papules and plaques that form superficial vesicles leading to a characteristic “honey colored” or “golden” crust. The lesions are often asymptomatic, but may be pruritic.
Diagnosis Clinical suspicion. Bacterial culture can be helpful
Pathology Superficial infection of the skin with Strep. Pyogenes or Staph. aureus. Often occurs after minor skin trauma.
Principles of Therapy Topical
mupirocin or systemic antibiotics (
dicloxacillin, cephalexin, erythromycin).
Description and SymptomsRecurrent self-limited tender vesicular eruption most often found on the lips and genitalia. Prior to the recurrence, a tingling or burning sensation is usually felt.
Diagnosis Appropriate history and clinical appearance. Culture or PCR may be used.
Pathology Herpes Simplex Virus 1 - mostly oral.
Herpes Simplex Virus 2 - mostly genital.
Principles of Therapy Antivirals (
famcyclovir, acyclovir, valacyclovir) taken at the first sign of recurrence may abort or shorten an episode.
Description and Symptoms Folliculits presents as one or many red papules (and pustules) originating from a hair follicles. Larger, tender nodules are termed furuncles. Multiple follicles may be involved (carbuncle).
Diagnosis
Pathology
Infection, usually by Staph aureus, of a hair follicle.
Principles of Therapy
Antibacterial soap, antibiotics topical (
mupirocin, clindamycin) or systemic (
dicloxacillin, cephalexin, erythromycin). PRN I&D. Warm compresses.
Description and SymptomsSmall to large subcutaneous nodules with an overlying plugged follicular opening (punctum) almost anywhere on the body. Occasionally inflamed due to traumatic rupture of the cyst sack or superinfection.
Diagnosis Clinical diagnosis
Pathology Blocked follicular opening leading to accumulation of degenerated hair in the follicle (like a balloon)
Principles of TherapyNo therapy indicated unless for cosmetically bothersome or symptomatic (repeatedly inflamed/tender). Surgical removal is the only option.
DISEASES All diseases caused by dermatophytes are called tinea coming from the Latin word for worms. That’s because the Romans thought it was worms getting into your skin. They are then named after the place they infect so T. capitas is the head, T. corporis – body, T. cruris – crotch, T. manum – hand, T. pedis – feet, T. unguium – nails. Over 50% of people will be infected in their lifetime; it is the second most common disease, and over $200,000,000/yr are spent on cures.
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T. pedis the most common tinea (30- 70%). It starts off mild and then can go into remission or into secondary bacterial infection which looks really really gross. T. pedis only started being such a problem in the last 200 years because of people wearing tight, non-airy shoes. It’s more common in adults and in people with a genetic predisposition. Caused by T. rubrum, mentagrophytes, and E. floccosum. The treatment is creams, and if that don’t work then systemic antifungals.
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T. unguium starts off in a corner and spreads, sometimes even to other toes. Usually caused by T. rubrum. The only effective treatment is systemic antifungals for several months and monitor liver functions. 5-10% of the population get it.
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T. capitas scalp infection, usually caused by microsporum and trichophyton. Mostly affects young people and African Americans. The incidence has been decreasing, probably due to better sanitary conditions. The infection smells like urine and mouse droppings. There are infections that are anthrophilic and live inside the hair shaft and other live on the outside. They weaken the hair and cause it to break. Prevention includes avoiding oiling or braiding hair, not sharing combs or hats, going to clean barbers, avoid overcrowding, skin trauma, and animals. Treatments over the years have been really weird. In Paris, they covered the head with tar and then pulled it off. Then they used X-rays but that led to baldness and brain tumors. Now we use azoles for 2-4 weeks or griseofulvin for 6-8 weeks.
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T. cruris affects the groin and perineum, usually caused by T. rubrum, and E. floccosum. Usually men get it. It spares the penis and scrotum. It can be prevented by using loose cotton clothing, sterilize towels and underpants, and losing weight. It’s treated with topical and systemic antifungals.
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T. corporis caused by T. rubrum, and T. mentagrophytes. People have it and scratch the lesions and pass it on to other parts of the body. The middle of the lesion is smooth and the edge is bumpy due to an immune response.
There are skin infections that can be confused with dermatophytic infections. These include T. versicolor is caused by yeast. It makes someone have spots that are darker or lighter than thir skin and comes out in the sun. Candida will be dealt with later. Sebhorreic dermatitis is probably caused by an exaggerated T-cell response to yeast. Eczema is an immune response seen in 10-20% of the population, especially babies. Psoriasis is scaling, thickening, and inflammation of the skin.
Diagnosis:
The doctor takes a scraping or clips the nail adds KOH and ink, this melts keratin, but don’t harm the hyphae adds fluorescent coloring if there’s fungi they stand out under UV light. In the lab it grows slow at low temperatures. Chloramphenicol is added to kill bacteria and cyclohexinide to kill fast growing fungi. Then the lab looks at the plates, but interpretation is varied and experience is needed. On DTM plates, dermatophytes form red halos because they change the pH. An important thing to know for the boards is that they used to use a wood lamp (which is a UV light) and hold it to the hair. If the hair fluoresces then it’s a fungal infection.
a. Primary Syphilis --
painless chancre
b. Secondary syphilis -- maculopapular rash, condylomata lata (flat topped papules -- located at the anus and in skin folds where heat and moisture exist).
c. Rocky Mountain Spotted Fever -- stage 1: erythema chronicum migrans (a red rash that spreads, leaving a clear center -- bulls-eye rash).
d. Meningococcemia --intravascular multiplication of N. meningitidis in the blood can result in a petechial rash (minute hemorrhagic spots the size of a pin that do not blanch when pressed). The rash can enlarge if the organisms multiply in the blood to the leading to fulminant meningococcemia (Waterhouse-Friderichsen syndrome--bilateral hemorrhage into the adrenals).
e. Herpes Zoster (varicella zoster) Virus -- vesicular rash (chicken-pox) that appear on the back of the head and ears then spread to the face, neck, trunk, and extremities. The distinguishing feature from other rashes (small pox) is that lesions will be at different stages (whereas small pox lesions are concentrated on the extremities and are all in the same stage). The lesions are very pruritic (itchy).
f. Coxsackievirus --Coxsackie A: herpangina -- fever, sore throat, and small red-based vesicles over the back of the throat. Hand-foot-mouth disease -- (coxsackie A-16) eruptions of small pearly, gray vesicles on the fingers, toes, palms, and soles often accompanied by painful vesicles and ulceration of the buccal mucous membranes and the tongue with slight fever; disease lasts 4 to 7 days.
