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Dermatology panic


Bullous acantolytic dermatosis (loss of adhesion of epidermal cells) - The antibodies are directed against desmosomal antigens and adhesive molecules of cold cadherins which condition the adhesion of spinal cells.
Subepithelial bullous dermatosis Antibodies are directed against particular components of the basal membrane zone(BMZ) or anchoring fibres lying below.
Pemphigus vulgaris The most common variant is vulgaris, which presents with flaccid blisters and erosions. These may be anywhere, but in over 50% of patients the mouth is affected and perineal lesions are also common. The blisters rupture easily. Just above basal layer.
Pemphigus foliaceus Pemphigus foliaceus does not always present with obvious blisters, because they are even more fragile than in pemphigus vulgaris: there may only be non-specfic scaly areas, and scalp and face involvement closely simulate seborrheic dermatitis.
Nikolsky sign Positive when slight rubbing of skin results in exfoliation of the outermost layer. Almost always present in toxic epidermal necrolysis and is ass w pemphigus vulgaris. Useful in diff betw pemphigus vulgaris (positive) and bullous pemphigoid (absent)
Investigations for pemphigus Biopsies from inv skin, preserving an early blister, Perilesional tissue for direct immunoflu. Serum for indirect immunoflu. Bright staining around epidermal cells w antibodies dir against IgG and C3 and circ antiepithelial antibodies in most patients.
To diagnose bullous disorders - Tzank Test - scrape ulcer base to look for tzanck cells, multinucleated giuant cells. Nikolsky Sign DIF (antigens) IIF (antigens)
Characteristics of pemphigus vulgaris - The most severe type - Skin and mucosa are involved - Mucosaa lesions usually precede skin lesions even few months. - Location – no predilection - Course chronic, afebrile
Pemphigus vegetans Immunologicly subtype of PV - Presence of hypertrophic foci in the regions of natural openings, folds - Skin and mucosa membrane involved
Pemphigus foliaceus Less severe type - Very slow progression - Mucosa membrane is not involved
Pemphigus erythematous Subtype of PF - Seborrhoic and hyperceratotic crusts or erythemato-squamous lesions on the face similar to SLE.
Char phenomena of pehmphigus Deposition of immunoglobulins in the epidermo-dermal junction like in SLE - ANA can be present.
Therapy of pemphigus Corticosteroids (prednison 100-120mg/day) – the dose is reduced when new blistering has ceased. - Immunosupression - Cyclophosphamid (Endoxan), azathioprine, chlorambucil, methotrexate Monoclonal antibody - rituximab Sulphons
Herpes Gestationis Deposits complement, rarely IgG. Erythemato-oedemato-vesicular lesions (like BP) w pruritus +burning of skin. No symptoms of eclampsia. Hormonal factor – onset during pregnancy, remission after baby, provoced during intake of hormonal contraceptive.
ARA criteria for diagnosis of SLE MD H SOAP RAIN. Malar rash, Discoid lesions, Hematological disturb (hemolytic anemia), Serositis (pleuritis), Oral ulcers, Arthritis Photosensitivity, Renal dist, ANA, Immunological (dsDNA, anti-Ss), Neurological (seizures).
How many ARA criteria do we need to diagnose SLE? 4 out of 11 SLE is likely. If it is 2-3 out of 11: Lupus-like disease.
Helpful diagnostic in SLE Raynaud phenomenon - Alopecia - Serum complement decreased - Positive DIF at dermo-epidermal junction (lupus band test)
Lesions of discoid lupus Light-exposed areas (face, neck)+dorsa of hands +arms. Sunlight may precip or worsen. Lesions: scaling, red plaques, prominent follicular plugging. Heal w scarring. Active, red, scaly margin around central area of scarred, hypopigmented, atrophic skin.
Diagnosis of discoid lupus Confirmed by skin biopsy (ANA mainly undetected) - Direct immunofluorence of lesional skin reveals granular deposists of IgG and/or IgM at the dermoepidermal junction
Treatment of discoid lupus Potent fluorinated topical steroids (if ineff, intralesional injection of triamcinolone or oral therapy w antimalarial hydroxychloroquine). If severe, oral steroids. Vit PP (Niacin). Disseminated DLE with much hyperkeratosis – aromatic retinoids.
General SLE multisystem disorder: skin, joints, heart, pericardium, lungs, kidneys, brain and hematopoietic system. Women of childbearing age. Mucocut lesions include oropharyngeal ulceration, diffuse alopecia, Raynauds phenomenon, vasculitis and photosensitivity.
Subacute cutanous lupus erythematosus – Non-scarring, papulosquamous or annular lesions occur predominantly on light-exposed areas. Associated systemic features may occur, but are usually mild. Antibodies to the RO and SSA antigen are characteristic findings.
Neonatal lupus erythemoatous Ass w transplacental passage of maternal anti-RO and anti-La antibodies. Skin lesions, thrombocytopenia, hepatosplenomegaly and complete heart block. Heart block persists, other features resolve as maternal antibodies disappear from the infants blood.
Scleroderma general Means “thickening of the skin” ,applied to a group of disease in which there is sclerosis of the skin and destruction of hair follicles and sweat glands. Predominantly expressed by: - Vascular changes - Immunological disturbances - Fibrotic disturbanc
Types of scleroderma Systemic scleroderma - disseminated systemic scleroderma and limited systemic scleroderma (CREST)
Treatment of fibrosis in scleroderma Fibrosis - Penicylamine – inhibits the proliferation of fibroblasts. INFγ – inhibitor of collagen production. Calcitriol – inhibits the proliferation of fibroblasts, collagen production. UV therapy – production of collagen. also use vasc and immunosup
Immunosuppressive drugs in scleroderma Immunosupressive drugs - Endoxan - in progressive dSSc (cyclophosphamide) - Cyclosporine A - Corticosteroids – very severe cases - Cyclophosphamide for IPD and bosentan for pulomary hypertension.
Treatment of vascular scleroderma Vascular changes - Calcium canal blockers - Dextran - ACE inhibitors is of significant benefit in renal disease. - Vitamin E, Piascledine
Morphea Localized scleroderma. Isolated patches of hardened skin, gen no internal organ involvement. Disorder of unknown etiology in which there is sclerosis of the skin. Dermatoms localisation – role of nervous system. Associated with borrelia burgdorferi
Circumscribed morphea most common – solitary or multiple indurated plaques develop, predominatly on the trunk. The surface is smooth and shiny. The sclerosis resolves, leacing atrophic, hyperpigmented areas.
Linear morphea one limb, often extending full length. In childhood it can significantly impair growth of the limb, and produce severe flexion deformities of large joints and digits.
Treatment of morphea Treatment – penicillin, vitamin E, piascledine, CS, calcitriol analogues, calcineurin inhibitors, UVA and methotrexate.
Dermatomyositis Autoimmune inflamm disease of skin + muscle, in childhood (5-14) or adult life (50-60). Symmetrical weakness +wasting of proximal muscle groups -> difficulty combing hair or standing up. Also IPF and cardiac disease (conduction defects)
Note when dermatomyositis - In adults in 50% connected with neoplasm
Types of dermatomyositis Dermatomyositis - Type of polymyositis - In adults in 50% connected with neoplasm - Mi 2 (ANA) – benign form of DM, good respond to corticosteroid therapy - Jo1 (ANA) – connected with the involvement of lungs
Diagnostic criteria of dermatomyositis Proximal, symmetrical weakness of shoulder and pelvic griddles muscles - Bushy capillaries of nail fold. - Myopathy i histopathology of the muscle - Myopathy in EMG - Elevated levels of muscle enzymes (Creatyne kinase (MM form)Aldolase)
Juvenile dermatomyositis Acute form is more frequent Vasculitis and late development of calcinosis are features of childhood disease No association with neoplasm More frequent calcinosis of soft tissue
Treatment of dermatomyositis Treatment include corticosteroids and immunosuppression (azathiprine, methotrexate or cyclophosphamide)
Varicella Zoster Virus Red spots over the whole body, small papules, vesicles, pustules Scalp is regularly affected, hands and feet are almost free Subsequent impetiginisation Severe itching, scaring. dorsal root ggl.
Herpes Zoster Herpes zoster (shingles) is an acute, selflimiting, vesicular eruption occurring in a dermatomal distrubiution (most ofte non thorax or abdomen)
Zoster Shingles Erythematous maculopapules, in 12-24 hrs become vesicles, grouping over erythematous base. Unilateral band or grouped vesicles on erythematosus base. In 48 hours -> pustsles, dry up, crusts in 7-10 days. Crusty last from 2-3 weeks (resolves in 2-3 weeks)
Zoster generalisatus Occurs in 2-5% of zoster patients Particularly in older patients Initial segmental distribution, generalised eruption Paraneoplastic syndrome: indicate the presence of tumour
Zoster-complications 2ndary bact infect: Local lymphadenopathy, Motor palsy, Post herpetic neuralgia - esp in elderly (pain in dermatome after lesion have healed) - Ophthalmic disease, ocular damage (keratitis, corneal perforation, uveitis) - Zoster encephalitis, meningit
Cellulitis Bact infect of subcut tissues. In immunolonormal is caused by S.pyogenes. The organisms may gain entry into the skin via minor abrasions. area becomes red, hot and swollen, and blister formation and areas of skin necrosis may occur. Fever, feels unwell.
Predisposing factors for cellulitis A frequent predisposing factor is edema of the legs, and cellulitis is a common condition in elderly people, who often have leg edema of cardiac, venous or lymphatic origin.
Treatment of choice for cellulitis Penicillin is the treatment of choice, initially given as benzylpenicillin IV. If the leg is affected, bed rest is an important aspect of treatment. Where there is extensive tissue necrosis, surgical debridement may be necessary.
Necrotizing fasciitis Esp severe, deep form of cellulitis, inv fascia +muscles. Ass w extensive tissue necrosis and severe toxemia and is rapidly fatal unless urgent treatment including excision of the affected area is undertaken.
Erysipelas superficial streptococcal cellulitis that has a well-demarcated edge. It is an acute, erythematous, rapidly spreading skin infection, associated with systemic symptoms. Typical localization is face and legs. There are different types:
Complications of erysipelas Recurrent erysipelas - Elephantisis – due to lymphatic damage during active phase - Celullitis - Lymphangitis and thrombophlebitis
Treatment of erysipelas Benzylpenicillin IV or Amoxicillin (erythromycin) − Bed rest and elevation of affected limb. And if more severe surgery. − Ichtyol topically
Staphylicoccal diseases Folliculitis - Sycosis staphylogenes - Furunculus, furunculosis, carbunculus - Staphylococcal scalded skin syndrome SSSS
Folliculitis inflammation of the opening of the hair follicle or superficial part of a hair follicle with S.Aureus produces a small pustule on an erythematous base, centered on the follicle. Mild: topical antibiotic agents, but if extensive a systemic AB may be req.
Treatment of folliculitis Topical - Antibiotic aerosols (neomycine, tetracycline, bacitracine) Systemic - Antibiotics based on antibiotics sensitivity profile - Sulphonamides
Sycosis staphylogenes Chronic folliculitis - Long – lasting (months, years) - Can promote scarring Very difficult and long-lasting treatment
Treatment of sycosis staphylogenes Very difficult and long-lasting treatment - Antibiotics: topical and systemic - Sulphonamides - Vitamins (B, C) - Hygiene
Furunculosis (boil) A boil is the result of deep infection of a hair follicle by S.Aureus. A painful abscess develops at the site of infection and over a period of a few days becomes fluctuant and points as a central pustule. Gradually resolves.
Recurrent boils or furunculosis Patients suffering from recurrent boils should have swabs taken from the nose for culture, and if found to be carrying staphylococci should be treated with a topical antibacterial such as mupirocin, applied to the nostrils.
Locations of boils Common locations: nape, face, axilla, buttocks, arms, legs Danger locations: middle face (cavernous sinus thrombosis), upper lip.
Therapy for furuncles (boils) Therapy Topical - Drawing ointments: ichthyol and Povidone-iodine Systemic - Antibiotics: penicillinase-resistant penicilline, cephalosporins Surgical – Incise, puncture
Carbuncle Carbuncle – deep infection of a group of adjacent hair follicles- Nape of the neck and trunk is a frequent area. The worst form of furuncle. Therapy is systemic antibiotics (flucloxacillin) and drainage.
Carbuncle therapy Carbuncle – deep infection of a group of adjacent hair follicles- Nape of the neck and trunk is a frequent area. The worst form of furuncle. Therapy is systemic antibiotics (flucloxacillin) and drainage.
Impetigo contagiosa Common superficial skin infect char by blisters that rapidly rupture -> honey colour crusts. More common in children and is highly contagious (epidemics in kindergartens) Typical localisation is face, groin, facial region, heal without scarring
Treatment of impetigo contagiosa In localized infection, treatment with topical antibiotics, such as mupirocin will suffice, but in more severe and extensive infection, treatment with systemic antibiotics (flucloxacillin or erythromycin is indicated).
Types of fungal infections Dermatophytes – ”ringworm infections” - Yeast-like fungi - candidia - Phycomycetes
Dermatophyte infection dermatophyte grow only in keratin – stratum corneum of the skin, hair and nails. Tinea pedis most common.
Tinea Pedis Most common dermatophyte infections. Scaling, itchy areas in the toe webs, esp betw the 3rd and 4th, and 4th and 5th toes or on the soles. Infected keratin debris on floors of swimming polls and showers. Smts extensive inv of soles and sides. Asymm inv.
Tinea Pedis serious Occasionally, athletes foot follows a pattern of episodic vesiculobullous lesions on soles, warm weather. The feet are frequently asymmetrically involved in fungal infection, in contrast with eczema, in which the inv is usually symmetrical.
Tinea unguium Toenail fungal dystrophy is very common and is ass with athlete’s foot. Usu starts laterally as yellowish streaks in nail plate, but gradually the whole nail becomes thickened, discolored and friable. T.Rubrum usu cause.
Nail mycosis usually infection starts on the free nail plate margin thickening, fragility, hyperkeratosis, yellow, brown or green colour very often are observed reccurences
BCC Most common malign. Usu begin as nodule, spreads slowly outwards, leaving central depression. Transparent, pearly, usu has teleangiectatic vessels - contact bleeding. Metas v ratre, local invasion, can spread along bony passages into skull. Sun-exposed.
Clinical forms of BCC: - Nodular BCC - Ulcerative BCC - Morphea like BCC - Cystic BCC - Superficial BCC - Pigmented BCC
Treatment of BCC Treatment: - Excision, biopsy, radiotherapy - Superficial tumors: curettage, cryotherapy or photodynamic therapy
SCC – in situ (Bowen disease) – is an SCC confined to the epidermis and is common below the knees in elderly women. Invasive change does occur, but is rare. - Solitary patch pf red scaly skin, although multiple areas may occur - Asymptomatic
Erythroplasia of Queyrat Noninvasive dysplastic changes on penis, clinical appearance of velvety red plaque. May occur on light-exposed skin and non-exposed skin. Treated by excision, curettage, cryotherapy or photodynamic therapy; very large areas may require radiotherapy.
Invasive SCC Skin cancer derives from spinous cell layer of epidermis. It is less common than BCC, but can metastasize to regional lymph nodes and beyond (especially lip, mouth and genital lesions). Associated with HPV virus infection (especially in genital area).
Clinical forms of SCC Ulcerative SCC - Verrucous SCC – rapidly growing polypoid mass - A keratotic lump - Can developed everywhere, most typically border of the skin and mucous membrane.
Prognosis of SCC Prognosis depend on proportion of atypical forms of the cells – BORDERS scale: 1 stage < 25% atypical cells 2 stage 25 – 50% 3 stage 50 – 75% 4 stage > 75%
Dermatitis Herpetiformis Most frequent bullous disease in children. Ass w gluten-sensitive enteropathy. Intense itching and grouped erythematous papules and vesicles. Usu on elbows + extensor surfaces. Most freq bullous disease in children. Anat change in small intestine.
Treatment of dermatitis herpetiformis Treatment are sulfones and glutenfree diet.
Urticaria Group of diseases char by formation of wheals – swelling of skin that disappear leaving no visible sign. Dermal edema due to vascular dilatation and incr permeability, often in resp to histamine from mast cells.
Clinical features of urticaria the skin itches or stings; wheals develop, white at first, then pink with a white rim; lesions can become very extensive and appear in many sites at once, but always clear spontaneously within a few hours, even though new lesions may continue to develop
Acute urticaria attacts last only a dew hours or days. Common causes include: - Nettles, animal fur or foods - Nuts, shellfish and strawberries - Ingestion of drugs (aspirin or penicillin) - More common WITH ATOPY AND ALLERGIES
Primary lesions of urticaria The primary lesions – raised wheals with blanching center, an erythematous flare associated with itching. Develops quickly (due to mediators), they vary in size (from few mm to several cm), their number ranges from few to manu appearing each day.
Classification of urticaria Allergic – most frequent – stops when inciting agent is removed - Physical – dermographism, cold, heat, sun exposure, pressure and water - Cholinergic – small intensely itchy papules that appear in response to sweating - Contact - Ass with vasculitis
Dermographism most common form of physical urticaria. Red dermographism: dev on stroked skin after 15-20 sec.(vasodil). Urticarial dermographism: 3-5 min after a pressure stimulus- mech induced release of histamine. This is usually in nervous people and in under stress
Cholinergic urticaria Induce by emotional, exercises or spicy food - Disseminated, highly pruritic small wheals/papules on erythema - Occur most frequently on the upper part of the body (upper thorax and neck) - IgE- dependent urticaria Eruption lasts few minutes to an hou
Chronic urticaria Attacks last for weeks, months or years. - Chronic recurrent: free intervals of a few or many days, > 4 weeks, up to many years - Chronic continous: new wheals daily, >4 weeks, up to many years
Treatment for urticaria Treat pot cause: infect, metabolic alterations, Give H1 antihistamines or inhibitor of mast cell degranulation or complement activation Combination H1 and H2 blockers Glucocorticosteroids --- 3-7 days Specific hyposensitization: bee or wasp venom al
Superficial mycosis of scalp (tinea capitis) Childhood. Fungi resp for scalp ring worm vary. Patches of partial hair loss. Scalp is scaly, hair broken off just above surface. Very contagious. Smts point to seborrheic dermatitis. Hair loss not perm, no scarring.
Open comedones dilated blocked hair follicles. It is not clear what causes the characteristic black dots. Blackheads are virtually pathognomonic of acne in the younger patient.
Rosacea central cheeks, forehead, end of nose and chin. The eruption consists of small papules and pustules arising in crops on erythematous, teleangiectatic background. No comedones.
Treatment of rosacea Treatment of choice is tetracyclines and oral metronidazole. Severe resistance may respond to oral isotretinoin.
Treatment of acne topical - Tretinoid - Benzoyl peroxide - Erythromycin and clindamycin Systemic – tetracycline’s, erythromycine, isotretinoid, UV, salicylic acid, oral contraceptives
Main symptoms of gonorrhea The main symptoms are - Pain and burning on urination - Purulent urethreal discharge - Yellowish and sometimes bloody vaginal discharge - Bleeding between periods
Erythema multiformae Target lesion: multiforme is the target lesion (a round or oval area of erythema, with a dusky, purplish centre. Sometimes the centre becomes paler and blister forms). Acute onset, enlarge over days – symm inv. Palms, soles, genital, oral. poor cond.
Predisposing factors for Candidiasis diabetes, GI diseases, pregnancy, obesity, antibiotic therapy, immunosuppression, steroid therapy, microinjuries, sweating, profession (soldiers, dish-washers).
Mucous membrane candidiasis oral cavity or genital area. The white, curd-like plaques adhere to the mucosa. If these are scraped off, the underlying epithelium is inflamed and friable. White patches with itching or burning sensations. Nystatin, ketoconazole.
žSkin candidasis (intertrigo candidamycetica) Lim to skin folds. Clinically – erythematously exudative focuses with irregular border, papules and pustules.
Treatment of skin Candidiasis Therapy with combined topical preparation containing an anti-candida agent, such as miconazole.
Nail candidiasis Chronic inflamm process affecting the proximal nail fold and nail matrix. First lesions are observed on the proximal nail fold which is inflammated and painful (purulent lesions), then are observed nail plate changes (grey or yellow colour, delamination
Malignant melanoma Developes from melanocyte. - 90% of cases on the skin, rarely can developed in an eyeball, meniges, mucous membrane. - Can developed from previously existing naevi or rarely from unchanged skin
Lentigo maligna melanoma (LMM) Patch of malig melanocytes in sun damaged-skin, proliferate radially along dermoepidermal junct and deep around hair follicles. Almost always face. LMM is invasive component of LM. More common in old pat (F), size 1 – 3 cm. Long lastin course of disease
Superficial spreading melanoma (SMM) - Most frequent type of melanoma. Typical location are trunk, limbs, neck and sun-exposed areas. Clinically slightly elevated lesion, spreading circumferentially, multicolour (brown, black, blue, white), asymetric border
žNodular melanoma (NM) - Second most common form. The most agressive. Location trunk, head, limbs. Can developed from pigmented nevous or unchanged skin. It has a fast growth.
žAcral lentiginous melanoma (ALM) – typically is located on the palms and soles. White race suffers from if rarely. It is a large lesion, sometimes with ulceration. There is a rapid progression. Subungual (under nail) melanoma
žMucous melanoma – sometimes defined as ALMM – acral lentiginous mucosal melanoma. Most common on the mouth and lips, can appear on the genital area, anus, urethra and oesophagus
Staphylococcal Scalded Skin Syndrome, SSSS Uncommon. Certain staph prod a toxin, splits epidermis at level of granular layer. Superf epidermis peels off in sheets, -> scalded skin. Infants and young child. Flucloxacillin. Fever, rash in diaper area, body covered by large flaccid blister that easil
Pemphigoid More common. Old. Limbs. When bullae develop they are usually numerous, tense, dome-shaped and may be filled with blood. When blister burst, healing is usually rapid. Some blisters do not burst, and the fluid is simply reabsorbed. Scarring is rare.
Diagnosis for pemphigoid requires - Biopsy for histopathology - Biopsy for direct immunofluorence - Serum for indirect immunofluorence
Treatment of pemphigoid Both variants require treatment with systemic steroids, in moderate doses, usually with immunosuppressives such as azathioprine or chlorambucil ( in severe cases and CP) - Tetracyclinum and niacine - Corticosteroids (prednizon 30-60mg/day) - Sulphons
Topical treatment of psoriasis Steroids - Calcitriol - Tar - Salicylate/urea/lactate - Anthraline (slows cell division – antimitotic) - Tacrolimus - Phototherapy (311nm – 290-320), UVB, PUVA (320-400)
Systemic treatment for psoriasis Acetretin – pustular type (vitamin a) - Isotretinoin – most effective in pustular psoriasis. - Ciclosporin Methotrexate Etanercept, Infliximab and adalimumab Systemic steroids rapidly clears psoriasis, but it may relapse and get worse (rebound eff
Scabies Small 8-leg mite. Common in children. Female scabies mite burrows in epidermis, lays eggs in the burrow behind her. After a period of 4-6 weeks, hypersensitivity to the mites or its products dev, itching, worse at night. Lesions: burrows and scabies rash.
Norwegian scabies SCABIES – crusted scabies – immunocompromised. Lesions are often markedly hyperkeratotic and/or crusted (itchy psoriasis). Lymphadenopathy. Milion of infesting mites
Diagnosis of scabies To diagnosis scabies – microscopy, dermoscopy, dermatopathology and eosinophilia.
Treatment of scabies PERMETHRIN 5 % CREAM - pregnancy - LINDANE - CRITAMITON 10 % CREAM - SULFUR 2 – 10 % in petroleum – the safest ! - Malathion 0.5% lotion - IVERMECTIN p.o. (single 400 mg dose) Treat family.
Nontreponemal serologic test for syphilis (STS) Mesures IgG and IgM directed against cardiolipin – lecithin – cholesterol antigen complex.
Steven Johnson syndrome subtype of erythema multiforme w inv of mucus membranes. Ccute, severe inflamm of conjunctiva, mouth and genitalia, may prevent normal eating, affect micturition and cause ocular scarring. Pat can die of severe bronchopulmonary involv or renal failure
Created by: angelshair