group 2 sy a, sy j, sydiongco, tacata, tady, tamondong, tan e, tan g, tan m, tan s

Group 2 Sy A, Sy J, Sydiongco, Tacata, Tady, Tamondong, Tan E, Tan G, Tan M, Tan S

SY, Aaron Keefe S.

FIXED DRUG ERUPTION recur at the same site with each exposure to medications Six or fewer lesions occur, frequently one May be present anywhere on the body, but half occur on the oral and genital mucosa

Clinical Features Begins as a red patch Evolves to an iris or target lesion identical to erythema multiforme that may eventually blister and erode Lesions of genital and oral mucosa presents as erosions Most lesions are 1 to several cm in diameter. New lesions may be added with continiued /repeated ingestion of the medication.

Pathophysiology Exact mechanism is unknown Recent research suggests a cell-mediated process that initiates both the active and quiescent lesions. Lesion contain intraepidermal CD8+ T-cells with the phenotypic markers of effector memory T-cells. Skin-resident T-cells rapidly produce IFN- on exposure to medication.

Histologic Features An interface dermatitis occuring with intraepidermal and subepidermal vesicle formation, necrosis of keratinocytes and a mixed superficial and deep infiltrate of neutrophils, eosinophils, and mononuclear cells. Stratum corneum is normal in acute stage. Papillary dermal fibrosis and deep perivascular pigment incontinence are commonly present from prior episodes.

Etiologic Agents Medications usually taken intermittently. NSAIDS, esp. Pyrazole derivatives, Paracetamol, Naproxen, Oxicams, & Mefenamic Acid predilection for the lips Sulfonamides, Trimethoprim or the combination resp. for majority of genital fixed drug eruptions

Possible Etiologic Agents Include: Barbiturates Tetracyclines Phenolphthalein (in laxative) Acetaminophen Ceterizine Celecoxib Dextromethophan Hydroxyzine Lamotrigine Phenylpropanolamine Erythromycin Chinese & Japanese herbs

Patch Testing needed to determine which drug may be involved Patch tests with various concentrations of the offending medication can reproduce the lesion on an affected but not unaffected skin. Most useful in pyrazolone derivative- related reactions.

Nonpigmenting Fixed Drug Eruption large, tender, often symmetrical eythematous plaques Resolve completely within weeks. Pseudoephedrine hydrochloride most common cause Baboon Syndrome buttocks, groin, axilla

Treatment Main goal - identify the causative agent and avoid it. Lesions of fixed drug eruption resolve spontaneously with avoidance of the inciting drug.

Sy, Jamelle D.

ERYSIPELAS St. Anthonys fire / ignis sacer an acute beta-hemolytic group A streptococcal infection of the skin involving the superficial dermal lymphatics group B perineal erysipelas

ERYSIPELAS local redness, heat, swelling, & a highly characteristic raised, indurated border PMN leukocytosis skin lesions: transient hyperemia vesicles or bullae legs and face are the most frequent sites affected

ERYSIPELAS septicemia, deep cellulitis, or necrotizing fasciitis complications: operative wounds, fissures, abrasions or scratches, unclean tying of the umbilical cord, venous insufficiency, obesity, lymphedema, and chronic leg ulcers predisposing causes: contact dermatitis from plants, drugs, or dyes, and with angioneurotic edema may be confused with:

TREATMENT Pharmacologic Vigorous antibiotic therapy for at least 10 days systemic penicillin erythromycin Non-pharmacologic Ice bags and cold compresses

CELLULITIS Sydiongco, Paula

Diffuse suppurative inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin Malaise, chills, fever, and toxicity may occur Lymphangitis, regional lymphadenopathy, or both may be present In severe cases, patients may develop hypotension and area infiltrated and pits on pressure

No racial and sex predilection No age predilection; individuals older than 45 years Facial cellulitis is more common in children younger than 3 years. Perianal cellulitis is predominantly a disease of children. Site of infection may occur anywhere on the body, but the leg is the most common site of the infection, followed by the arm, and then the head and neck areas. following surgery or trauma wounds, cellulitis can develop in the abdomen or chest areas. morbid obesity, it can also develop in the abdominal area

Incubation 24 hours or can take days to develop. Duration less than a week to disappear with antibiotic therapy. months to resolve completely in more serious cases and can result in severe debility or even death if untreated. Not properly treated, it may appear to improve but can resurface months or even years later.

break in the skin such as a fissure, cut, laceration, insect bite, or puncture wound Risk factors: tinea pedis; elderly and those with immunodeficiency; diabetic people; Immunosuppressive drugs; Chickenpox and shingles; chronic venous insufficiency and varicose veins; pregnancy and obesity Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis The vast majority of cases are caused by Streptococcus pyogenes or Staphylococcus aureus

Cellulitis S pyogenes Immunocompetent adults Perianal cellulitis (children) perianal erythema and pruritus, purulent secretions, painful defecation, and bleeding in the stools S aureus Children Pasteurella multocida dog or cat bite or scratch Pseudomonas aeruginosa after a puncture wound Nongroup A streptococci (ie, groups B, C, and G) lymphatic obstruction or venectomy for coronary artery bypass graft Aeromonas hydrophilia, Vibrio vulnificus after exposure to freshwater or seawater

Haemophilus influenzae cellulitis Haemophilus influenzae type B Children < 6 y.o. Rare in countries where vaccination is available Bacteremia may lead to meningitis, orbital cellulitis, osteomyelitis, or pyarthrosis Culture, needle aspirate Cefotaxime and ceftriaxone; Rifampin Pneumococcal facial cellulitis S pneumoniae Young children Extremity involvement: DM, subs. abuse Head, neck & upper torso involvement: SLE, nephrotic syndrome, hematologic dso. Fever, leukocytosis, and septicemia Penicillin, vancomycin

Helicobacter cellulitis Helicobacter cinaedi Fever, bacteremia, cellulitis and arthritis HIV- infected patients; malignancy, diabetes; and acoholism distinctive red-brown or copper color w/ minimal warmth Ciprofloxacin Tuberculous cellulitis Mycobacterium TB px taking chronic corticosteroids Past history of pulm. TB Four drug treatment

Diagnosis Cellulitis is most often a clinical diagnosis Blood cultures usually are positive only if the patient develops generalized sepsis Resemble Cellulitis: deep vein thrombosis: compression leg ultrasound Lyme disease has been misdiagnosed as staph- or strep-induced cellulitis (bullseye rash does not always appear): to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic. [2] [2]

Complications Gangrene Metastatic abscess Grave sepsis Children and compromised adults

Treatment & Prevention Rest affected limb & cleaning the wound site and treatment with oral antibiotics Early lesions: Intralesional inj of triamcinolone acetonide 1:10 Mild cellulitis: Flucloxacillin monotherapy (to cover staphylococcal infection) Moderate cases or where streptococcal infection is suspected: combined with oral phenoxymethylpenicillin or intravenous benzylpenicillin, or ampicillin/amoxicillin ; cefazolin or vancomycin

Severe cases: require admission and intravenous (IV) therapy. Wound: cleaned and dressed appropriately done daily or when they become wet or dirty Medical advice should be sought: wound deep or dirty and retained foreign bodies

TACATA, Patricia TADY, Clarissa Marie

URTICARIA (HIVES) characterized by wheals surrounded by a red halo or flare severe itching, stinging or pricking annular or polycyclic pattern clearing of central region and coalescence of lesions

URTICARIA (HIVES) Subcutaneous swellings (angioedema) may accompany the wheals target the gastrointestinal and respiratory tracts resulting in abdominal pain, coryza, asthma and respiratory problems.

ACUTE VS. CHRONIC URTICARIA days to weeks Produce evanescent wheals that rarely last >12h Resolution within 6 weeks of onset ACUTE Daily episodes of urticaria and/or angioedema lasting >6w Physical urticaria common CHRONIC

COMMON TRIGGERS Opiates Polymyxin B Tubocurarine Aspirin and other NSAIDS Tartrazine Benzoate

ETIOLOGIC FACTORS Most frequent cause of acute urticaria MOST COMMON: Penicillin and related antibiotics Allergic rhinitis or asthma, nasal polyps and food induced anaphylaxis A.DRUGS frequent cause of acute urticaria whereas in chronic urticaria food is a less frequent factor MOST COMMON: Chocolate, shellfish, nuts, peanuts, eggs and milk Serum radiallergosorbent tests(RASTs) can be used to detect specific IgE and elimination of diets can be of benefit. B. FOOD

ETIOLOGIC FACTORS Natural food additives: yeasts, salicylates, citric acid, egg and fish albumin Synthetic additives: azo dyes, sulfites, penicillin, benzoic acid derivatives With the exception of sulfite and penicillin, most food additives can be avoided by eating only meat produce and dairy products Packaged food are largely prohibited. C. Food Additives

ETIOLOGIC FACTORS Streptococcal infections Chronic viral infection (Hep B & C) Helminths (ascaris, ankylostoma,filaria) D. Infections Severe emotional stress no matter what the primary cause Initiating stimulus in CHOLINERGIC URTICARIA E. Emotional Stress Associated with carcinomas and Hodgkins disease F. Neoplasms

ETIOLOGIC FACTORS Grass pollens, house dust mites, feathers, formaldehyde, etc. G. Inhalants Induced by ingestion of alcohol H. Alcohol Rarely causes urticaria I. Menthol

PATHOGENESIS Capillary permeability Release of histamine from the MAST CELLS (PRIMARY EFFECTOR in urticarial reactions) Serotonin, leukotrienes, prostaglandins, proteases and kinins other substances that may cause vasodilation and capillary permeability

DIAGNOSIS Clinical grounds Fixed lesions >24h: Urticarial vasculitis, granuloma annulare, sarcoidosis, cutaneous T cell lymphoma Skin biopsy: if wheals last >24h CLINICAL EVALUATION Detailed history and physical examination Radiologic sinus evaluation Blood count to detect eosinophilia Review of medications in chronic urticaria Skin biopsy

ANAPHYLAXIS An acute and often life threatening immunologic reaction Scalp pruritus, diffuse erythema, urticaria and angioedema Most common causes of serious anaphylactic reactions: Penicillins, radiographic contrast agents Hymenoptera stings, shellfish and other food allergens

Treatment Acute Urticaria Antihistamines Non-sedating Histamines pose a lower risk of psychomotor problem in adults. Avoid the trigger if the cause can be identified Systemic corticosteroids For severe reactions, respiratory and cardiovascular support is essential. Intubation and tracheotomy may be required.

Chronic Urticaria Mainstay treatment: Antihistamines Should be taken on a daily basis and not prescribed to be taken as needed Second generation antihistamine produce less sedation in most patients Second line treatment Phototherapy Calcium channel antagonist Antimalarial medications Methotrexate Corticosteroids produce long term side effects Local treatment Tepid or cold tub baths Topical camphor and menthol

Angioedema Acute, evanescent, circumscribed edema Area of predeliction: Eyelids, lips, lobes of ears, external genitalia, or mucous membranes of the mouth, tongue, or larynx Swelling occurs in the lower layers of the skin or in the subcutaneous tissues Frequently begins during night and is found on awakening Two subtypes: Deep form Angioedema associated w/ C1 esterase inhibitor deficiency

Hereditary Angioedema (HAE) Quincke edema 2 nd 4 th decade, Autosomal dominant inheritance Swelling: Asymmetrical without urticaria or itching In subcutaneous tissues and abdominal organs mimicking surgical emergencies, and the upper airway (larynx) life-threatening Little response to antihistamines, epinephrine, or steroids High mortality rate death often caused by laryngeal edema 3 phenotypic forms: Type I Type II Type III Trigger factors: minor trauma, surgery, sudden changes in temperature, or sudden emotional stress

Acquired C1 Esterase Inhibitor Deficiency Usually occurs after 4 th decade of life No family history Not associated w/ pruritis or urticaria Two subtypes: A. Acquired angioedema-I Rare disorder associated with lymphoproliferative diseases Treatment: Replacement of C1-EI with concentrates or FFP; antifibrinolytic agents; synthetic Danazol B. Acquired angioedema-II Extremely rare disease Treatment: Immunosuppresive therapy; Synthetic corticosteroids (temporarily effective); Plasmapheresis

Episodic Angioedema with Eosinophilia Uncommon disorder w/ no underlying disease Isolated facial edema May occur with fever, weight gain, eosinoophilia and elevated eosinophil major basic protein Treatment: administration of systemic steroidal medications, antihistamines, and IVG

Schnitzler Syndrome Rare disorder Combination of chronic, non-pruritic urticaria, fever of unknown origin, disabling bone pain, hyperostosis, increased erythrocyte sedimentation rate, and monoclonal IgM gammopathy Age of onset: 29-77 years old; affects both sex Effective therapy has not been determined Bone pain and urticarial lesion respond to systemic corticosteroids

Physical Urticarias Occur most frequently in ages 17-40 years old Most common form dermatographism > cholinergic > cold urticaria Chronic idiopathic urticaria: Dermatographism, delayed pressure, cholinergic, and cold urticaria Other forms: Adrenergic Urticaria Vibratory Angioedema Heat Urticaria Aquagenic Urticaria Solar Urticaria Pressure Urticaria ( Delayed Pressure)

Dermatographism Sharply localized edema or wheal with a surrounding erythematous flare occurring within seconds to minutes after the skin has been stroked Affects 2-5% of the population Arise spontaneously after drug-induced urticaria and persist for months H 2 antihistamine may be of benefit

Cholinergic Urticaria Produced by the action of AcH on the mast cell Characterized by minute, highly pruritic, punctuate wheals or papules 1-3 mm in diameter and surrounded by areas of erythema Area of predilection: trunk and face Persists for 30-90 min and followed by a refractory period with no lesions of up to 24 hours Palms and soles are spared Trigger factors: exercise, emotional stress, increased environmental temperature, or intradermal injection of nicotine picrate or methacholine Treatment: adequate dosage of antihistamines; Danazol in refractory cases

Cold Urticaria Exposure to cold may develop edema and wheals on the exposed areas; usually on the face and hands Urticaria does not develop during chilling but on rewarming Types: Primary no underlying systemic disease - Tx: Doxepin, Cyproheptadine; Acrivastine and Cetirizine Secondary - Associated with underlying systemic disease such as cryoglobulinemia Familial Cold Urticaria- produces a Burning sensation with cyanotic centers and surrounding white halos lasting for 24 48 hrs - Leukocytosis - Tx: Stanozolol therapy

Tamondong, Roxanne Tan, Ernie Joe

Erythema Multiforme Erythema multiforme minor Herpes simplex-associated erythema multiforme (HAEM) Strongly associated with preceding herpetic infection

Clinical features Self-limited Recurrent disease Young adults 1-4 weeks Sharply marginated, erythematous macules Raised, edematous papules 24-48 hrs

Classic target or iris lesion A ring of erythema that forms around the periphery, and centrally the lesions are flatter, more purpuric, and dusky 3 zones: Central dusky purpura Elevated, edematous pale ring Surrounding macular erythema Typical target lesions best seen in palms and soles

Lesions appear symmetrically and acrally Initial involvement most frequently of the dorsal hands Dorsal feet, extensor limbs, elbows, knees, palms and soles 10% of cases, more widespread lesions occur on the trunk Mucosal involvement in 25% of cases and is limited to the oral mucosa

Atypical HAEM Outbreaks of unilateral or segmental papules and plaques that may be few in number or solitary Lesions may be up to 20cm in diameter Plaques- erythematous and evolve to have a dusky center, which desquamates Subcutaneous nodules may be present

Histology: features of EM and HSV can be seen Acyclovir prevents the lesions Prednisone increase the frequency of attacks

Etiologic factors Preceding orolabial HSV infection Appear 1-3 weeks (average of 10 days) after the herpes outbreak Not all episodes of EM may follow every episode of herpes

Pathogenesis due to an allergic reaction(medication) or infection(HSV or Mycoplasma) involves damage to the blood vessels of the skin followed by damage to skin tissues. Activated T lymphocytes are present in lesions of Erythema Multiforme. Epidermis Cytotoxic or Suppressor cells Dermis Helper T-cells EM minor is linked to HLA type HLA-DQ3

Histopathology Histologic Features are NOT predictive of etiology due to similar feature from EM to TEN(Toxic epidermal necrolysis) Extent of epidermal involvement depends on the duration of the lesion and where in the lesion the biopsy is taken Biopsy- basket-weave stratum corneum - suggest acute process where in there was not enough time to produce abnormal keratin

Histopathology Vacuolar interface dermatitis is present with vacuoles and foci of individual cells necrosis out of proportion to the no. of lymphocytes Dermal infiltrate is largely mononuclear and tends to be primarily around the upper dermal vessels and along the dermo- epidermal junction. Eosinophils may be present but rarely prominent and not predictive of etiology

Histopathology of EM must be differentiated from the following: Fixed Drug Eruption Graft vs Host disease Pityriasis lichenoides Lupus erythematosus -deeper infiltrate -w/ eosinophil and neutrophils - papillary dermal fibrosis - melanophages around post- capillary venules -More compact stratum corneum -Epithelial disorder resembling Bowens Disease -w/ lymphocyte in every vacuole - w/ erythrocyte extravasasion - neutrophil margination within dermal vessels -Compact hyperkertosis - a deeper periadnexal infiltrate - dermal mucin and basement membrane thickening

Differential Diagnosis when Bullae are prominent: PemphigusBullous pemphigoid Paraneoplastic pemphigus - Prominent mucous membrane involvment - Lesions are small - erythema prominent at periphery of the bulla -May produce atypical target lesions - mucosal involvement - vacuolar interface dermatitis - appear very similar to EM major

Treatment Most cases are self limited and symptomatic treatment may be all that required -Anti-histamine, Moist compress, Topical anesthetics and Acetaminophen Prevention: Sunscreen lotion and sunscreen-containing lip balm prevent UVB induced outbeaks of HSV Therapy: Oral Anti-viral (acyclovir, valacyclovir or famciclovir) Dapsone antibacterial that inhibits synthesis of dihydrofolic acid - alternative drug when anti-virals are not effective Systemic Steroids control inflammation Intravenous Immunoglobulin to stop disease process

Genevieve Lynn C. Tan

Exfoliative Dermatitis Dermatitis exfoliativa Pityriasis rubra (Hebra) Erythroderma (Wilson Brocq)

Exfoliative Dermatitis Extensive erythema and scaling Entire body surface is dull scarlet Small, laminated scales No vesicles and pustules Extensive telogen effluvium

Etiology Result of generalization of preexisting chronic dermatosis (61%) Medications allopurinol, sulfas, gold, phenytoin, phenobarbital, isoniazid, carbamazepine, cisplatin, dapsone, mefloquine, tobramycine, minocycline, nifedipine and iodine Inadequate intake of branched chain amino acids in infants with MSUD Idiopathic

Etiology Sezary syndrome Generalized exfoliative dermatitis with intense puritus Leonine facies Alopecia Palmoplantar hyperkeratosis Onychodystrophy

Criteria for diagnosis of Sezary syndrome: Absolute Sezary cell count of at least 1000/mm3 CD4/CD8 ratio >10 Increase Lymphocyte count with evidence of T cell clone Chromosomally abnormal T cell clone

Etiology Hodgkins Disease Generalized exfoliative dermatitis Fever Lymphadenopathy Hepatosplenomegaly ESR

Histopathology Nonspecific Hyperkeratosis Mild acanthosis Focal parakeratosis

Treatment Drug-induced stop drug Application of mild corticosteroid after soaking and occlusion under sauna suit Acitretin, cyclosporin, methotrexate for psoriatic erythroderma Isotretinoin, acetretin, methotrexate for PRP Azathioprine and methotrexate for idiopathic erythroderma unresponsive to therapy

Tan, Marie Dolores Tan, Samantha

Hansens Disease Also known as LEPROSY Chronic, systemic, infectious disease caused by Mycobacterium leprae Granulomatous or neutrophelic lesions in different parts of the body like: Skin Mucous Membrane Nerves Anterior Segment of the Eye Bones Viscera

Hansens Disease Mycobacterium leprae Weakly acid fast Grows 32-35C Cultivated in mouse pads and armadillos Favors intracellular location Only bacterium to invade peripheral nerves Phenolic Glycolipid (PGL-1) unique to leprosy bacillus

Epidemiology 10-15 million worldwide Asia (Indian Subcontinent), Sub-Saharan Africa, South and Central America, Pacific Islands, and the Philippines Most cases in tropical and developing world More common in people who are of low economic status, w/ inadequate housing, unsuitable sanitation, poor nutrition, and lack of education

Epidemiology Men > Female Occurs in all ages Peak presentations in children aged 10-20 years old and in adults 30-60 years old Mode of transmission: controversial (respiratory route: infectious droplets from nasal secretions) Genetic susceptibility

PATHOGENESIS Patients immune reaction to the leprosy bacillus: critical element in determining the outcome of infection. TUBERCULOIDLEPROMATOUS GranulomasWell-formed, contain helper T-cells Poorly-formed, predominant suppressor T-cells Cytokine profileIFN-, IL-2IL-4, -5, and -10 prominent Cell-mediated immunityGoodDownregulated

DIAGNOSIS Identification of M. leprae in the affected tissue Skin biopsies Skin or nerve lesions Stain: visualize the bacillus with Fite-Faraco stain Slit smears Lesions and cooler areas of the skin Stain: acid-fast stain Multibacillary: organisms found on the skin smears Paucibacillary: negative skin smears (and 5 or fewer lesions) Serologic tests Detects antibodies against M. leprae-unique antigens (PGL-1) PCR detects small numbers of organisms in infected tissue

Diagnostic procedures Histamine Test Metacholine Sweat Test Skin Sensory Test Lepromin Test (Mitsuda Reaction)

Hansens Disease Presents with a broad spectrum of clinical diseases Exposure No clinical disease (Spontaneous cure) Develops clinical disease PaucibacillaryMultibacillary

Early indeterminate leprosy Insidous onset Slight prodromal symptoms Numbness first clinical manifestation First lesion is a solitary, ill-defined hypopigmented macule (sometimes erythematous) Succeeding lesions common: Cheeks, upper arms, thigh, and buttocks Peripheral Nerves not enlarged No plaques No nodules No or very few bacilli on biopsy

SPECTRUM OF HOST-PARASITE RESISTANCE in leprosy High resistanceUnstable resistanceNo resistance Tuberculoid (TT) Borderline Tuberculoid (BT) Borderline (BB) Borderline Lepromatous (BL) Lepromatous (LL) Lesions1-3FewFew or many asymmetrical ManyNumerous and asymmetrical Smear for bacilli 01+2+3+4+ Lepromin test 3+2+++0 HistologyEpithelioid cells decreasing Increasing histiocytes, foam cells, granuloma, xanthoma-like Nerve destruction, sarcoid-like granuloma

Tuberculoid leprosy Solitary, large, few (

Borderline tuberculoid leprosy Lesions are similar to tuberculoid lesions, but smaller and more numerous (>10-20) Satellite lesions around large macules or plaques Less hair loss Nerves slightly enlarged Common sites of lesion: face and limbs www.aifo.it/.../online/courses/lepdd

Borderline leprosy Small, numerous (but countable), cutaneous lesions Generalized, but asymmetrical lesions Erythematous, irregularly shaped, ill defined borders Erythematous plaques with islands of normal skin Swiss Cheese Appearance Nerves are slightly enlarged, thicker, and tender Anesthesia is only moderate www.aifo.it/.../online/courses/lepdd

Borderline Lepromatous Leprosy Numerous (too many to count), symmetrical lesions: macules, papules, plaques, and nodules Ill-defined outer border and sharply marginated inner border - Inverted saucer shaped or Punched Out Reverse configuration of tuberculoid type Nerve lesions appear later, enlarged, tender, or both Anesthesia is often absent www.aifo.it/.../online/courses/lepdd

Lepromatous Leprosy Numerous, symmetrical macules, papules, plaques, and nodules Lepromas (nodules) on the earlobes, nose, lips, eyebrows Little or no loss of sensation over the lesions No nerve thickening No changes in sweating Leonine Fascies Madarosis lateral thinning of eyebrows Nasal ulceration www.aifo.it/.../online/courses/lepdd

Treatment WHO Western Pacific recommendation

Reactional states Characteristic and clinically important aspect of Hansens disease Experienced by 50% of patients after institution of multidrug therapy Triggers: intercurrent infections, vaccination, pregnancy, vitamin A, iodides, bromide Severe, abrupt 2 Forms TYPE 1TYPE 2 Caused/Mediated By:Cell-mediatedImmune complexes Occur In:Borderline Leprosy (BT, BB, BL) Lepromatous patients (BL, LL)

Management of reactions Even though reactions may appear after drug treatment is instituted, it is not advisable to discontinue or reduce anti-leprosy medication. MILD REACTIONS No neurologic complications or severe systemic symptoms Supportive treatment, bed rest, aspirin or NSAIDs TYPE 1 REACTIONS Prednisone Clofazimine TYPE 2 REACTIONS (ENL) Thalidomide: drug of choice; potent teratogen Systemic corticosteroids

prevention BCG vaccination alone provides about 34% prevention against infection BCG + heat-killed M. leprae increases protection to 64% Treat active multibacillary patients and examine exposed persons on an annual basis to detect early evidence of infection Chemoprophylaxis in hyperendemic regions Once yearly multidrug therapy with single dose rifampin+minocycline+clofazamine

group 2 sy a, sy j, sydiongco, tacata, tady, tamondong, tan e, tan g, tan m, tan s

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