Welcome. Patient itch/ Itchy Rash-2 Prof. DOULAT RAI BAJAJ Professor & Chairman Dept. of...

Post on 22-Jan-2016

216 views 0 download

transcript

welcome

Patient itch/Itchy Rash-2

Prof. DOULAT RAI BAJAJ Professor & Chairman

Dept. of Dermatology

Goals of Presentation

At the end of presentation you would be able to:

1. Clinically evaluate a patient with itch or itchy rash

2. Make a working diagnosis

3. Manage it at the best

Review Last Presentations

Evaluation of a patient presenting with itchy rash

Aopic Derm, Sebh. Derm. Irritant Contact Dermatitis (ICD) allergic CD, Discoid, LSC, Prurigo, Pompholyx, P.rosea, P. alba, xerotic eczema

General Principles of treatmentPreventive measures

Tasks of Today

PsoriasisLichen PlanusScabiesPediculosisUrticariaDermatitis herpetiformis

PSORIASIS

Psoriasis

An autoimmune disease characterized by: Well defined, erythematous, plaques Bilateral Symmetrical distribution Silvery scales, varying thickness Predilection for Extensor aspects May be associated Joint involvement Runs a very chronic course with

remissions and relapses Auspitz Sign

Psoriasis contd….

May occur from infancy to very old age. Mostly b/w ages of 15 & 35 yrs

M: F affected equally. Same phenotype in both sexes

Koebner Phenomena: Psoriasis may develop @ sites of trauma, e,g, Scratch mark, Injury, Surgical incision, Friction from tight-fitting clothing/obesity Sun burn

Kobner Phenomena

Predisposing Factors:

Actual etiology unknown.

Genetic Factors Environmental Factors

Etiology:

Genetic factors

HLA Cw6Familial occurrence: 14% if one parent affected 41% if both parents affected 06% if one sibling affected 02% when no parent/sibling affected

Environmental:Trauma: Physical, Chemical, Electrical, SurgicalDry skinInfections: Streptococcal, HIVSunlight : may relieve or exacerbateHypocalcemia: Drugs: Lithium, Antimalarials, β-blockers,

NSAIDs, ACEIs, Terbinafine, Ca Chanel Block Withdrawal of corticosteroids Psychogenic factorsSmoking, Alcoholism

Clinical Types

Psoriasis vulgaris Guttate psoriasis Rupoid, Elephantine & ostraceous Unstable psoriasis

• Erythrodermic psoriasis • Pustular psoriasis

Psoriasis Vulgaris

Guttate Psoriasis

Generalized shower of small “rain drop” like deep red papules ē fine scaling.

Most common form in children.

Acute onset: Usually follow 3/4 wks off strept. pharyngitis.

Recurrent, b/c of pharyngeal carriage of streptococci.

Mainly trunk, sparing face, palms & soles.

04/21/23 33

Management It includesIt includes

General measures

Local therapy

Intralesional therapy

UV phototherapy

Systemic therapy

Lasers

04/21/23 34

GENERAL MEASURES

Attention should be paid to general, physical & psychological health.

Rest & mild sedation

Stress alleviation

Stop smoking, alcohol, drugs

Spa therapy

DIET

04/21/23 35

Local Therapy

Keratolytics: salicylic acid

Tar: 2-10%

Dithranol: 0.05-4%

Corticosteroid

Vitamin D analogue: calcipotriol, calcitriol, tacalcitol

Vitamin A analogue: Tazarotene

Topical tacrolimus

04/21/23 36

Photo chemotherapy

Combination of psoralens & UVA.

Moderate to severe psoriasis.

It is one of the standard treatment b/c: Effective, long term effect. ORAL 8-MOP = 0.6 mg /kg or 5-MOP UV radiation/laser light 2 hours later UVA dosage depends upon skin type.

frequency: 2-4 times weekly (for 15-25 min.).

Systemic therapy

MethotrexateHydroxyureaOral retinoids: Etretinate

IsotretinoinAcetretin

Cyclosporin Systemic steroids. Biological Therapies

Methotrexate

MOA: Inhibits DNA synthesis by inhibiting DHFR

Start ē 7.5-15 mg/wk in single/divided × 3, given 12 hrly over 36 hrs. Inc 2.5 mg every 2-4 wk, Max: 30mg/wk

Folic acid supplement 5mg daily (on days without Mtx)

Monitor ing Monitor ing : : Hepatic, renal & marrow function. Routine liver biopsy.

Avoid concurrent therapy ē NSAIDS, sulpha, ASA & Septran b/c they displace MTX from plasma albumin

Ciclosporin Antilymphocytic, inhibition of T-lymphos. Start with 2.5 mg/kg BID, for 2 wks. No response

to 5mg/kg/day. Use for short courses of 3-4 months.

S. ES. E. . Renal toxicity. HTN Malignancies: CIN (females), PIN (males), cut.lymphoma Hypertrichosis Gum hyperplasia Biochemical: serum K+, serum uric acid. serum Mg+

Retinoids: Etretinate & Acetretin Synthetic analogues of Vit. A.

Acitretin is active metabolite of etretinate, ē ½ life of just 50 hrs VS ≥ 80 days for etretinate.

Best results when combined ē UVA (PUVA) Dose: 0.7-1mg/kg/d

Protocol: Protocol: Contraception during & up to 2 yr after stopping Rx. Lipid profile & LFT, CBC ē platelets, Renal profile

Lichen planus

LICHEN PLANUS A chronic papulosquamous disorder

characterized: plane toppedPolygonalPurple papuleswhich are highly pruritic Surface may show white lines: Wickham’s Stria

Etiology: Exact etiology unknown. Genetic, immunological

Plane topped polygonal purple color papules

Papules appear in group

Size ranges from pinpoint to centimeter

SITESMost common sites: wrists, lumbar

region & around ankle. May occur any where on body

Ankles & shins are the most common sites for hypertrophic LP

Hypertrophic lesions around ankle

Hypertrophic lesions present on shin

MUCOSAL INVOLVEMENTMucosal lesions very common, mostly

seen on buccal mucosa & tongue. White lacy streaks on inner surface of the cheeks, gum margins and lips: a very common finding

Mucosal Lesions includeWhite streaksFixed white patchesUlcerative lesionsStreaks of pigmentation

LP involving buccal mucosa

Lesion present on inner surface of cheeks

White streaks present on lips

White streaks on tongue

Drug Induced LP:

COMMON INDUCERS

Gold saltsβ-blockersAntimalarialsThiazide diureticsFrusemideSpironolactonepenicillamine

LESS COMMON INDUCERS

ACEIs

Calcium channel

blocks

Ketoconazole

Tetracyclines

Phenothiazine

CLINICAL & H/P Difference b/w IDIOPATHIC & DRUG induced LP

PRESENTATIONS IDIOPATHIC LP Drug Induced

lesions Smaller Larger and scally

Wickhams striae Usually present Usually absent

Alopecia Uncommon Common

Residual hyperpigmentation

Possible common

MM involvement Very common Less common

Parakeratosis Not seen common

Cystoid in granular layer

Very common common

TREATMENT

TOPICAL STERIODS:Flucinonide 0.05%Clobetasol propionate 0.05%

FOR PRURITIS:Promethazine HCLTrimeperazine tartrateBrom-pheneramine maleate

TREATMENT

SYSTEMIC STEROIDS: Oral prednisolon 15-20mg/d for about 6

wks for severe cases.

For cutaneous and erosive LP Acetretin Itraconazole Metronidazole PUVA

TREATMENT

FOR ORAL LESIONS: Lidocain gel triamcinolone in orabase Corticosteroids lozenges Betamethasone mouth washes Fluticasone propionate spray

Oral or systemic CYCLOSPORIN used to treat

ulcerative form of LP

Scabies

Scabies

Caused by Sarcoptes scabiei var humanis

Acquired through close personal contact (not

casual), but may be transmitted through clothing,

linen, furniture or towels.

Sexual transmission as common as non-sexual

Suspect scabies when several members of a

family complain of itching

Clinical Features: The IP <1 month (max: 2 months)

Severe itching: prominent symptom Nocturnal Pruritus first noticed 3-4 wks after primary infection,

but occurs sooner after subsequent attacks. May be localized initially to burrow, but later

becomes generalized. Burrow is the diagnostic lesion: Multiple straight or S-

shaped ridges or dotted lines resembling thread, 5-20 mm long

Sites:

interdigital webs of hands

wrists, anticubital fossae, points of elbow

nipples

Around the umbilicus, lower abdomen

Genitilia

Gluetal cleft

Lesions on glans penis→ Characteristic in males

Infants & small children: lesions on palms, soles, head & neck.Generalized urticarial papules, excoriations

& eczematous changes common in childrenIndurated erythematous nodules, most

noticeable on male genitalia → more common.

Sec: bacterial infection: Impetiginization, furunculosis

DIAGNOSIS H/O of pruritis with nocturnal exacerbations.Positive family history.Distribution of lesions In doubtful cases confirm by microscopyPolymerase chain reaction has been

employed in difficult diagnostic and atypical cases.

Treatment

General Measures: Improve general hygiene frequent bathing Trim down nails avoid close contact with active caseObserve caution when caring/nursing

patient keep personal utensils and towels separateTreat all family members at a time

Drugs

Topical Treatment is the gold standard & very effectiveTopical Permethrin 5%: lotions, creamsGamma benzene hexa chloride: Benzyl benzoateSulphur 10%Malathione: NAOral Ivermectin: efficacy???

URTICARIA

Urticaria characterized by weals: transient, well-demarcated, superficial erythematous or pale swellings of the dermis, usually associated with itching

While angioedema is a transient swelling in deep dermis, subcutaneous & submucosal tissue.

•Usually painful •Poorly defined •pale or skin colour

Definition

Urticaria and Angioedema

Urticaria Angioedema

Urticaria not a single disease: A REACTION PATTERN mediated by HISTAMINE

Mast Cells/Basophils play cardinal role. Their activation by various factors/agents/stimuli with subsequent release of MEDIATORS leads to clinical symptoms/signs.

Acute urticaria & chronic urticaria are not single entity. Clinically it is useful to d/b the two to make proper clinical decisions.

PATHOGENESIS

CLASSIFICATION

classificationclassification

According to According to duration of diseaseduration of disease

According to According to clinical featuresclinical features

DURATION OF DISEASE Acute urticaria

≤ 06 weeks Cause can be found in in approx. 50%; by history Good prognosis

Chronic urticaria ≥ 06 weeks workup indicated often persistent

Chronic idiopathic urticaria - subset of chronic urticaria in which workup fails to pinpoint cause; diagnosis by exclusion; not homogeneous.

Start as itchy erythematous macules Wheal Pale to pink with surrounding red flare. Duration: few hrs to several days, no sequelae Very itchy but pts. tend to rub rather than scratch Size: few mm to many cms Shape: round ,annular, bizarre. Angio oedema associated ē 50% of cases Sites: face, eye lids lips, ears, neck, hands, feet,

genitalia, buccal, tongue, pharynx & larynx

ORDINARY URTICARIA

Acute ordinary urticaria: ≤ 6 weeks.

TypesAllergic

Non-allergic

A reaction B/W an allergen with specific IgE antibody bound to mast cell

Common in atopic persons with raised IgE levels

ALLERGIC URTICARIA (IgE mediated)

Penicillin Cephalosporin Insulin vaccines Blood products Bee and wasp strings

Substances causing urticaria

Foods causing AU

Lobsters, shrimp, crab Milk nuts Fish Beans Potato Carrots Spices Rice Banana Apple Orange

Non allergic Acute urticaria from ingested substances

may be non-allergic.

They are referred to as intolerance reaction.

Due to direct histamine release from mast cell

Substances causing non allergic urticariaDrugs Aspirin, Other NSAIDs Polymyxin, ciproxin, rifampsin ,vancomycin. Radio contrast media Plasma expanders General anaesthetic agentsInfections Epstein bar virus, Hepatitis B virus Strept. sore throat in children

Etiology: D/B Acute VS Chronic

Acute UrticariaDrugs

Foods

Food additives

Viral: Hep: A, B, C, EBV

Insect bites and stings

Animal dander and latex

Chronic Urticaria Physical factors

–Cold, heat, solar, pressure

Ch. Viral, bacterial, fungal infect

chronic yeast infection

autoimmune: SLE, DLE, DM, SS

Complement deficiency

Malignancies: Lymphoma, leukemia

Idiopathic

Initial Workup of Urticaria

Patient history URTIs: Sore throat, Sinusitis,

pharyngitis Arthritis Thyroid disease Cutaneous fungal infections UTI symptoms Travel history (parasitic infection) EBV infectious mononucleosis Insect stings Foods Recent transfusions Recent intake of drugs

Physical examSkinEyesEarsThroatLymph nodesFeetLungsJointsAbdomen

Lab: Assessment for Chronic Urticaria

Tests for selected patients Stool exam. for ova, parasites, giardia Blood chemistry profile Antinuclear antibody titer (ANA) Hepatitis B and C Skin prick tests (IgE-reactions) RAST for specific IgE

Initial testsCBC with differentialESRUrinalysis

Complement studies: CH50

CryoproteinsT3, T4, TSH, Thyroid

antibodies

Treatment: Pharmacologic Options

Antihistamines, othersFirst-generation H1

Second-generation H1

Antihistamine/decongestant combinations

Tricyclic antidepressants (eg, doxepin)

Combined H1 and H2 agents

Beta agonists Epinephrine 1:10,000; 0.5-1ml

S/C: angioedema, sever acute urticaria

Terbutaline

CorticosteroidsSevere acute urticaria

–avoid long-term use–use alternate-day regimen

when possibleAvoid in chronic urticaria

(lowest dose plus antihistamines might be necessary)

MiscellaneousPUVAHydroxychloroquineThyroxine

H1-Receptor Antagonists: Pros and Cons for Urticaria and Angioedema

First-generation antihistamines (diphenhydramine, hydroxyzine) Advantages: Rapid onset of action, relatively inexpensive

Disadvantages: Sedating, anticholinergic effects

Second-generation antihistamines (astemazole, cetirizine, fexofenadine, loratadine) Advantages: No sedation (except cetirizine); no adverse

anticholinergic effects

Disadvantages: Prolongation of QT interval; ventricular tachycardia (astemizole only) in a patient subgroup

Dermatitis Herpetiformis

Very pruritic condition Characterized by: crusted, excoriated papules and vesicles. Vesicles very seldom seen

Widespread on back of trunk, head, elbows Occur in all age 22 – 55 years Sites : Elbow, knee, shin, scapulae & buttocks Patient may have gastrointestinal symptoms OR systemic signs of gluten sensitivity/CD.

Dermatitis herpatiformisDermatitis herpatiformis

Pruritus with Systemic Diseases

Systemic Diseases

Thyroid: hypothyroidism, hyperthyroidism, Hashimoto’s thyroiditis

Ch. Liver Diseases: cirrhosis, CAH, PBC Renal : CRF especially with dialysisis Blood: Anemia, Polycythemia Metabolic: Diabetes, HIV, AIDS Malignancies: lymphoma, leukemia, internal

malignancies

Characteristic Features There are minimal cutaneous lesions If present; these are non-specific, no predilection

for site Mostly there are dry papules broken in centre OR

dispersed excoriations S/S of systemic diseases are Dominant in whole

clinical picture Some specific features may be seen (next slide) Prognosis depends upon the prognosis of

underlying disease

Specific features of Systemic Ds Liver Ds: xerosis, diffuse melanosis, red palms, spiders,

gynaecomastia(males), edema, icteric Diabetes: xerosis, loose wrinkled skin, acanthosis, skin

tags, pyodermas, carbuncles, candida Renal: xerosis, uremic frost, perforating lesions, calcinosis,

vasculitic lesions Thyroid: xerosis, alopecia, madarosis, wrinkling in Hypo;

general flush, sweaty palms, angiomas, fine atrophic skin in Hyperthyroidism

AIDS: prurigo, urticaria, SD, cutaneous & mucosal candida Blood: general pale, lethargic look in anemia,

suffused, congested bronze skin in polycythemia

See This presentation @

www.lumhs.edu.pk/DFHC/html

THANK YOU