Module 5 - Clinical examination for STIs & RTIs

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Rotator Lecture VI:

Rotator Lecture VI Drug Eruptions, CTD, NF, MF

Exanthematous Drug Eruptions:

Exanthematous Drug Eruptions Most common manifestation of drug reactions Presents as erythematous macules and papules coalescing into diffuse erythema Skin may peel as rash is resolving Most common causes include sulfa, PCN, and PCN derivatives

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Figure 23.1 Exanthematous drug eruptions. Numerous pink papules on the trunk due to a cephalosporin (A). Confluence of lesions on the trunk (B) and annular plaques on the forehead (C) secondary to phenobarbital. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Figure 23.1 Exanthematous drug eruptions. Numerous pink papules on the trunk due to a cephalosporin (A). Confluence of lesions on the trunk (B) and annular plaques on the forehead (C) secondary to phenobarbital. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Usually worst on LE due to orthostatic pressure.

Fixed Drug Eruption:

Fixed Drug Eruption Occurs in the same place each time a patient is challenged with a particular drug Round or oval lesion with an ash gray to slate blue colored center, may have bullae Can have 1 lesion or multiple Common causes include laxatives, NSAIDs, sulfa drugs, tetracyclines

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Figure 23.11 Fixed drug eruptions. Well-demarcated erythematous (A) to violet-brown plaques that can develop a detached epidermis Responsible drug was phenophthalein (A) Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

Erythema Multiforme (EM):

Erythema Multiforme (EM) This has many causes, drug eruption is one etiology Erythematous target-like lesions Minor variant does not require hospitalization Usually a reaction to HSV infection Major variant (Stevens-Johnson) requires hospitalization and immediate treatment

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Figure 21.1 Phenotypic variety in EM. D classic target lesions on the palms . Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

Stevens Johnsons Syndrome (SJS) and Toxic Epidermal Necrosis (TEN):

Stevens Johnsons Syndrome (SJS) and Toxic Epidermal Necrosis (TEN) SJS and TEN always caused by a drug More severe than EM Involves mucosa SJS arbitrarily defined as involving at least 2 mucous membranes and having at least 10% body surface area involved TEN is worst end of spectrum with more severe cutaneous and mucosal manifestations and can be fatal

SJS and TEN:

SJS and TEN Common causes include antiepileptics, sulfa drugs More severe than EM SJS: Rapid course, large sheets of necrotic skin, can involve mucosa, evolves within days; can rapidly turn into TEN (hrs) TEN: Extremely rapid course. Evolves within hours. Can be fatal! Treat patient in burn unit, administer IV Ig, plasma pheresis Oral/systemic steroids have not been able improve mortality (can increase susceptibility to infection)

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Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Figure 21.6 Denuded and crusted lesions of the lips with minimal cutaneous lesions in a child with SJS secondary to antibiotic therapy. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Figure 21.7 Severe conjunctival erosions and exudate in SJS secondary to trimethoprim-sulfamethoxazole therapy. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Figure 22.6 Stevens-Johnson syndrome (SJS) versus SJS-TEN overlap. In addition to mucosal involvement and widespread erythematous papules, there are small areas of epidermal detachment (arrows). Because the latter involve 10% body surface area, the patient is classified as having SJS. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Figure 22.5 Clinical features of toxic epidermal necrolysis (TEN). A Detachment of large sheets of necrolytic epidermis (>30% body surface area), leading to extensive areas of denuded skin. B Hemorrhagic crusts with mucosal involvement. C Epidermal detachment of palmar skin. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

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Figure 22.4 Cutaneous features of toxic epidermal necrolysis (TEN). A Characteristic dusky-red color of the early macular eruption in TEN. Lesions with this color often progress to full-blown necrolytic lesions with dermo-epidermal detachment. B Positive Nikolsky sign: epidermal detachment reproduced by mechanical pressure on an area of erythematous skin. Downloaded from: Dermatology (on 29 June 2006 07:55 PM) © 2005 Elsevier

TEN:

TEN

Urticaria:

Urticaria Has many causes! Pressure, exercise, food, temperature, and drug Transient lesion (<24 hours), new ones can form with continued contact Resolve without scarring Remove offending agent(s), administer anti-histamines

Angioedema:

Angioedema severe form of urticaria involving dermis and subcutaneous swelling which can affect airway, mucosa, and bowels. Can be from food, medication, latex allergy

Angioedema:

Angioedema Can occur simultaneously with urticaria Angioedema without urticaria can also occur Drug reaction C1 esterase inhibitor deficiency JAAD 2002; 46: 645-57.

Angioedema: Drug Reactions:

Angioedema: Drug Reactions ACE Inhibitors Often orofacial angioedema Urticaria/angioedema is believed to result from the inhibition of endogenous kininase Can occur up to 1 yr after starting med NSAIDs Aspirin

Angioedema: Drug Reactions Management:

Angioedema: Drug Reactions Management Withdrawal of drug Antihistamines, corticosteroids Epinephrine may be needed if airway in trouble or very severe Report of FFP used in refractory case (to above and IVIg, CSA)

Hereditary Angioedema:

Hereditary Angioedema Autosomal dominant; with incomplete penetrance 1:150,000 Mutations in one copy of the gene for C1 inhibitor Type 1: reduced levels of C1 inh (85% of cases) Type 2: functionally deficient C1 inh (15% of cases) C1inh deficiency allows activation of the C1 generation of bradykinin subsequent consumption of complement leads to low levels of C4 in the serum

Hereditary Angioedema:

Hereditary Angioedema Trauma can precipitate attacks Attacks last 48-72 hrs Laryngeal edema Abdominal pain NO WHEALS (ie NO URTICARIA)

Hereditary Angioedema:

Hereditary Angioedema Fitz 6 th ed p 1132

Acquired Angioedema:

Acquired Angioedema Type 1 C1 fixed by anti-idiotypic antibodies causes consumption of C1 inh Seen in lymphoproliferative disease, esp. multiple myeloma, Waldenstroms, B cell lymphoma, CLL Type 2 autoantibodies (IgG1) against C1 inh Associated with SLE, RA, Sjogren’s

Angioedema (only) work-up:

Angioedema (only) work-up Medications: Avoid estrogens FH C4 : BEST SCREEN Screens both hereditary and acquired C1 inhibitory deficiency C1q Low in acquired C1 inh def. C1 inh assay Amount: type 1 deficiency Function: type 2 deficiency

Hereditary Angioedema: Rx:

Hereditary Angioedema: Rx C1 inh concentrate of FFP For emergencies Tranexamic acid (IV) FDA approved for hemophilia antifibrinolytic agent: competitively inhibits the activation of plasminogen to plasmin Danazol, Stanozolol: treatment of choice

Acquired Angioedema: Rx:

Acquired Angioedema: Rx Secondary to lymphoproliferative disease Stanozolol Danazol Secondary to anti-C1Inh autoantibodies Respond to glucocorticoids

Dermatomyositis:

Dermatomyositis Combination of skin and striated muscle inflammation Characteristic Skin Manifestations: Heliotrope Rash Gottron’s papules/sign Poikiloderma (atrophy, telangectasia, and pigmentary alteration) Muscle Manifestations Symmetric proximal muscle weakness Elevation of skeletal muscle enzymes (CPK, aldolase) EMG, muscle biopsy, and MRI can also be used to confirm myositis

Heliotrope: periorbital edema with a lightly violaceous hue:

Heliotrope: periorbital edema with a lightly violaceous hue

Gottron’s Papules:

Gottron’s Papules Pathogmonic for Dermatomyositis Erythematous-violaceous scaly papules over dorsal IP joints, elbows, or knees Gottron’s sign are patches or plaques of the same color in the same distribution Photosensitivity is the proposed etiology Associated with proximal nail fold atrophy and telangiectasia

Gottron’s papules:

Gottron’s papules

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Figure 44.4 Gottron's sign with violaceous poikiloderma over the knuckles. Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

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Figure 44.2 Violaceous poikiloderma of the face, plus thin plaques on the elbows (Gottron’s sign) that are sometimes misdiagnosed as psoriasis. Downloaded from: Dermatology (on 29 June 2006 09:20 PM) © 2005 Elsevier

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Figure 44.1 Violaceous poikiloderma of the face. Heliotrope also noted. Downloaded from: Dermatology (on 29 June 2006 09:20 PM) © 2005 Elsevier

Dermatomyositis:

Dermatomyositis Up to 25% are associated with underlying malignancy Ovarian cancer is overrepresented in women Patient’s with new diagnosis need cancer screening at diagnosis and yearly

Scleroderma:

Scleroderma Disorder characterized by fibrosis of connective tissue, increased collagen deposition, and vascular alterations. Localized disease without systemic manifestations is called “morphea” or “localized scleroderma” Systemic disease with skin manifestations is called “systemic scleroderma” Subsets of this are CREST and systemic sclerosis ANA is not helpful in diagnosis

Localized form of morphea: ‘en coup de sabre’:

Localized form of morphea: ‘en coup de sabre’

Limited Systemic Sclerosis: CREST:

Limited Systemic Sclerosis: CREST

Sclerodactyly seen in CREST:

Sclerodactyly seen in CREST

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Figure 45.3 Mat telangiectasias in a patient with systemic sclerosis (scleroderma). Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

Progressive Systemic Sclerosis:

Progressive Systemic Sclerosis Skin thickening is more widespread and proximal Can be severe and rapidly fatal Both CREST and PSS can causes renal disease and pulmonary sclerosis

Cutaneous Lupus:

Cutaneous Lupus ACUTE: Typical photosensitive malar rash when acute Highly associated with systemic LE (almost 100%) SUBACUTE: This variant is psoriasiform or papulosquamous ~50% of these patients will meet criteria for SLE CHRONIC: ie Discoid Lupus Most patients (85-90% never develop systemic lupus)

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Figure 43.4 Acute cutaneous lupus (ACLE) lesions in a butterfly distribution on the face of a young woman. Note sparing of nasolabial folds. Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

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Figure 43.5 Acute cutaneous lupus (ACLE). The patient shown in this photo had ACLE lesions on the arms as well as the face. Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

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Figure 43.7 Subacute cutaneous lupus (SCLE) lesions of the sun-exposed aspects of the upper arm. Note the annular configuration and crusting of the borders. Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

Discoid Lupus Erythematous (DLE):

Discoid Lupus Erythematous (DLE) Most scarring and chronic form of cutaneous lupus Discoid shaped plaques with white scale, with time, lesions become atrophic Can lead to scarring alopecia Few patients meet criteria for SLE Treat with intralesional or topical steroids, sun avoidance, plaquenil if severe or large areas involved

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Figure 43.9 Chronic cutaneous lupus erythematosus (CCLE) with discoid lesions. The ear is a common site of involvement. Note the central depigmentation, scarring and peripheral hyperpigmentation. Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

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Figure 43.10 Chronic cutaneous lupus erythematosus (CCLE) discoid lesion. Downloaded from: Dermatology (on 29 June 2006 08:28 PM) © 2005 Elsevier

Neurofibromatosis :

Neurofibromatosis Type 1 (vonRecklinghousen) is more common that Type 2 Autosomal dominant inheritance in half of cases, other half are spontaneous Hereditary form has variable penetrance; can be associated with mental retardation Some Criteria: 2 or more neurofibromas, 6 or more café au lait macules, Lisch nodules in the eyes, Axillary or inguinal freckles (Crows sign)

Mycosis Fungoides (MF) :

Mycosis Fungoides (MF) Most common type of cutaneous T-cell lymphoma NOT A FUNGAL DISEASE! Most common in middle-aged white men Occurs in patch and plaque stages Asymmetrical distribution of lesions Treat with steroids, UVB, nitrogen mustard, PUVA, methotrexate, retinoids, interferons

Patch vs. Plaque Stages of MF:

Patch vs. Plaque Stages of MF Flat Fine white scale Erythematous ‘Cigarette paper’ wrinkling Serpiginous or annular Non-specific rash, can resemble psoriasis or eczema Localized Red to violaceous nodules Associated with lymphadenopathy Alopecia Hyperkeratosis of palms and soles Widespread Lesions can become ulcerated

Thank You!:

Thank You!

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