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Eczema (Dermatitis)

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Dermatology

‫د. سهام‬

Tuberculosis (TB) of the Skin
- Invasion of the skin by mycobacterium tuberculosis. - The route of infection & the immunity of the individual determine the variety of cutaneous tuberculosis that develops in a patient. Classification (No entirely satisfactory system of classification exists): 1. Primary TB (tuberculous chancre). 2. Secondary TB.

Secondary TB
1. Localized TB; the infection here results from inoculation of the skin by the microorganism either directly from outside the body (exogenous) or as an extension from an underlying tuberculous process: a. Lupus vulgaris. b. Scrofuloderma. c. WartyTB. d. Orificial TB. 2. Generalized TB; the infection here results from inoculation of the skin by the microorganism that reaches the skin by the blood from distant focus in the body (haematogenous). a. Acute miliary TB. b. Tuberculous gumma . c- Tuberculides (eruptive TB).

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Primary TB Tuberculous Chancre
This is very rare, results from direct inoculation of the skin from outside in an individual who does not have naturally or artificially acquired immunity to this organism. The site is any exposed area, and the lesion consists of small symptomless papule that eventually ulcerates. Also gross associated regional lyrnphadenitis occurs that proceeds to caseation (primary complex). The condition occurs chiefly in children and heals spontaneously within 6-12 months.

Secondary TB 1- Localized TB Lupus Vulgaris
-This is the commonest variety of cutaneous TB. The mode of infection in the majority of cases is through exogenous inoculation of the skin by TB bacillus in a person with a moderate or high degree of immunity, in others it occurs by lymphatic spread from the mucous membranes of the nose or throat & rarely by haematogenous dissemination especially when we have multiple foci. -The conditions usually affects children, females are affected as twice as males. Any part of the body may be affected, but the face and particularly the nose are the sites mostly affected. -The characteristic lesion is a reddish-brown plaque composed of nodules called apple jelly nodules because of their pale brownish-yellow appearance. -This plaque extends irregularly in some areas, while in others scarring occurs causing considerable tissue destruction over many years.

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-The apple-jelly nodules are characteristic and are more easily visible by diascopy (vitropression) ie. gentle pressure on the lesion with a transparent glass slide to impede local blood flow, the lesion then becomes white and the apple- jelly nodules appear as small brownish spots. The other characteristic thing is that new active lesions may develop in the scar giving the name “unhealthy scar” Deformities of the nose (beak nose), mouth (microstomia) & eyelids (ectropion) may be produced and carcinoma may occur in old-standing lesions of lupus vulgaris, SCC & less commonly BCC. Differential Diagnoses: 1. Lupus crythematosus: usually affects middle-age group, lesions are redder, no apple jelly nodules, and the presence of the characteristic stippling in LE (produced by the filling of the orifices of the sweat glands & hair follicles with little horny lugs). 2. Tertiary syphilis:occurs in older people, nodules are bigger and not present on the healed scar. When the nose is attacked, syphilis affects the bones rather than the cartilage leading to saddle-nose. 3. Cutaneous Leishmaniasis: course is shorter, smears & culture reveal the causative org.s (protozoon leishmania tropica ). 4. Tuberculoid leprosy: loss of sensation over the esions and resemble grains of sand rather than apple-jelly

Scrofuloderma
The skin overlying a tuberculous lymph node or a joint may become involved in the process. This variety is most commonly seen in the neck. The skin over the tuberculous area becomes stretched, indurate Fed and a little bit elevated. With time it will open by multiple sinuses, discharging sero- puru!ent & caseous material. Around these sinuses, many ulcers develop with characteristic undermined bIuish edge. Eventually healing will take place with treatment leading to scar formation & disfigurement of the area. Such patients usually have fair degree of immunity against infection.

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Warty TB
(tuberculosis verrucosa cutis) - The patient is usually having a high degree of immunity against the infection. The site of the skin lesion is usually exposed area, but the dorsurn - The lesion starts as a small, indurated,( symptornless– warty papule that tends to spread very slowly with tendency for central healing.

Orificial TB
- Usually develops in patients with minimum degree of immunity, especially thoses with advanced pulm.TB. - It results from auto- inoculation of miro-org through expectoration from the lung or the mico- org. being swallowed, then the micro-org. either b inoculated in the mouth, nose or around anal orifice. The resultant skin lesion is in the form of multiple nodules that soon ulcerate giving rise to multiple, painful, shallow irregular ulcers which are difficult to heal .

2- Generalized TB Acute Miliary TB
An acute haematogenous dissemination of Tb. Which still chiefly affects infants & children especially following measles. Its manifestations are profuse crops of bluish papules, vesicles, pustules or haemorrhagic lesions in a patient who is obviously ill. Such patients have minimal immunity against the infection.

Tuberculous Gumma
This form of TB is the result of: hematogenous dissemination from a primary focus during periods of bacillaemià & lowered resistance. It is
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seen particularly in poorly nourished children. The tuberculous gumma starts either as a firm sub-cut. nodule which slowly softens, or as an ill- defined fluctuant swelling. The overlying skin gradually breaks down with subsequent changes resembling those of scrofuloderma. The extremities are more often affected than trunk.

Tuberculides (Eruptive TB)
These are reasons f of various types that represent all allergic response of the skin to the tuberculous bacilli reaching it through the blood in patients with considerable degree of immunity against the disease. Micro-organisms are not found in the lesions.

A. popular tuberculides:
1. Papulonecrotic tuberculid: Present with crops of dusky red papules on the extremities. 2. Lichen crofulosorum: Is sometimes seen in children & young adults with disseminated form of Tb. The lesions are not very prominent, consisting of groups of lichenoid papules often showing. a perifollicular distribution; usually seen on the trunk. These gradually regress over a period months.

B. Nodular tuberculides:
1. Erythema induratum (Bazin’s disease): Is found exclusively in women. Lumpy indurated lesions, very dark in color, develop around the ankles & legs and may break down into ragged-edged shallow ulcers with a notably indolent course. Although evidence of Tb. elsewhere in the body is lacking, the patients show a high degree of tuberculin sensitivity and the lesions respond to treatment with anti-TB Drugs. 2- Erythema nodosum. 3- Nodular vasculitis. The last two are less clinically-specific forms.
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Diagnosis:
1- Clinical history & signs. 2- Presence of active proven TB. elsewhere in the body. 3- Presence of AFB in the lesion. 4- Histopathology. 5- Positive reaction to tuberculin. 6- Effect of specific therapy. The above are relative, unreliable criteria for the diagnosis, but the absolute diagnosis is the positive culture of M. tuberculosis from the lesion.

Treatment
The new strategy of treatment of tuberculosis in general is the Directly Observed Treatment Short course (DOTS). Patients are, according to their clinical presentation, classified into three categories IN WHICH Cutaneous Tuberculosis is classified Under category III.The treatment policy for this category includes two months of intensive phase therapy(daily observation) & four months of continuation phase (weekly observation). Using only letters for the drugs used, the treatment will be like this.....2HRZ/4HR. the letter H is for TNH (isoniazid) (isonicotinic acid hydrazide) 5mg/kg/day, R is for rifampicin 10mg/kg/day & Z for pyrazinamide 25mg/kg/day. INH remains the standard drug to be given in all regimes for its efficacy, cheapness & low toxicity. Remember that any of the three drugs may cause hepatitis.

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Leprosy
Also named Hansen’s disease: A chronic infectious (in some cases) disease caused by mycobacterium leprae (acid-fast bacillus non- cultivable in vitro), primarily affecting peripheral nerves and secondarily involving skin & certain other tissues. inhalation of nasal droplets from cases of lepromatous leprosy. The incubation period is from 3-5 years. The range of clinical manifestations & complications depends upon the immune status of patients. Those with high resistance tend to develop the tuberculoid leprosy & those with low resistance develop the lepromaous type. Between the extremes lies a spectrum of reactions classified as “borderline”

Tuberculoid leprosy
1- The patient is highly resistant to the infection. 2- The infecting org.s are very difficult to be found in the lesions. 3- The patient is non-infectious. 4- Lepromin test is (+ve). The typical lesion of tuberculoid leprosy is a large erythernatous plaque with its clear-cut and elevated border that slopes down to a flattened atrophic centre. The lesion occurs commonly on the face and its surface is dry, hairless, insensitive sometimes scaly (skin appendages are damagedby the process). Less commonly, macular lesions develop which are usually single or few in number. They are well defined, asymmetrically positioned & hypopigmented (never depigmented) lesions. Nerves may be thickened near sites the skin lesions or a thickened nerve trunk may be felt in the vicinity, for instance thickened ulnar nerve if the lesion is on the arm. An area of anaesthesia & motor weakness may develop corresponding to the distribution of the thickened nerve.

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Lepromatous leprosy
1- The patient has minimal resistance to the infection. 2- The infecting org.s are present in high numbers in the lesions. 3- The patient is infectious. 4- Lepromin test is (-ve). Usually manifests as very numerous, small, symmetrical macules which posses normal sensation and have smooth erythematous surfaces and indefinite edges. The more characteristic papules, nodules & plaques appear later in the course of the disease. Changes on the face lead to what is called Leonine faces. Nerve affection appear late in the course of the disease. Upper respiratory mucosa may be involved leading to ulceration & epistaxis (nasal mucosa). The-eyes, testicles &also some other tissues may also be involved.

Diagnosis:
The diagnosis of leprosy should be considered in any, patient with skin or peripheral nerve lesions who is living in an endemic area especially if skin or nasal symptoms persist. despite routine treatment. 1- Two important clinical findings are pathonomonic: a. Anaesthetic skin lesions: A chronic lesion which may or may not be hypppigmented with impairment of sensation hair growth. b. Nerve affection: Thickening of a main nerve trunk in its superficial course, or of a branch close to the cutaneous lesion. 2- Positive smears (skin, nasal mucosa) for acid-fast bacilli. 3- Skin & nerve biopsy. Diagnostic histological findings are: a. Acid-fast bacilli in dermis &/or nerves.
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b-Tuberculoid changes in cut. or peripheral nerves. 4- Lepromin test for identification of the type.

Treatment:
Tuberculoid forms are usually treated for 6-12 months, while lepromatous leprosy needs, treatment for at least two years. Tuberculoid leprosy has a tendency for spontaneous limitation 1-Paucibacillary disease: Treated with dapsone (diamino-dipheny sulphone) lOOmg/day (1-2mg/kg) & rifampicin 600mg once monthly(supervised and not self- administered as with dapsone). 2-Multibacillary disease: Triple drug therapy is required Dapsone, rifampicin & clofazim. ine(a bacteriostatic agent with anti-inflammatory properties), which is given 300 mg once monthly supervised and 50 mg/day self-administered. A brief period of isolation is necessary only for patients with lepromatous leprosy until treatment renders them non-infectious (takes four days with rifampicin).

Haval Lutfalla Sadraddin®
hawlermedicine.jeeran.com

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Lingjuan Ma Lingjuan Ma
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