Transcript Zinc: another miracle micronutrient

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 treatment
 Preventive measures

Tasks of Today
Psoriasis
 Lichen Planus
 Scabies
 Pediculosis
 Urticaria
 Dermatitis 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
Etiology:
Actual etiology unknown.
Predisposing Factors:
Genetic Factors
Environmental Factors
Genetic factors
HLA Cw6
 Familial occurrence:

14%  if one parent affected
 41%  if both parents affected
 06%  if one sibling affected
 02%  when no parent/sibling affected

Environmental:
 Trauma:
 Dry
Physical, Chemical, Electrical, Surgical
skin
 Infections: Streptococcal, HIV
 Sunlight : may relieve or exacerbate
 Hypocalcemia:
 Drugs: Lithium, Antimalarials, β-blockers,
NSAIDs, ACEIs, Terbinafine, Ca Chanel Block
 Withdrawal of corticosteroids
 Psychogenic factors
 Smoking, 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.
Management

It includes
General measures
Local therapy
Intralesional therapy
UV phototherapy
Systemic therapy
Lasers
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GENERAL MEASURES
Attention should be paid to general,
physical & psychological health.
Rest & mild sedation
Stress alleviation
Stop smoking, alcohol, drugs
Spa therapy
DIET
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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
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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.).
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Systemic therapy
Methotrexate
 Hydroxyurea
 Oral retinoids: Etretinate

 Isotretinoin
 Acetretin
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 :

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. 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:

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
topped
 Polygonal
 Purple papules
 which 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
SITES

Most 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 INVOLVEMENT
Mucosal 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 include

White streaks
 Fixed white patches
 Ulcerative lesions
 Streaks 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
salts
 β-blockers
 Antimalarials
 Thiazide diuretics
 Frusemide
 Spironolactone
 penicillamine
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 HCL
 Trimeperazine tartrate
 Brom-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 Sshaped 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 children
 Indurated 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 microscopy
 Polymerase 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 case
 Observe caution when caring/nursing
patient
 keep personal utensils and towels separate
 Treat all family members at a time

Drugs

Topical Treatment is the gold standard &
very effective
Topical Permethrin 5%: lotions, creams
 Gamma benzene hexa chloride:
 Benzyl benzoate
 Sulphur 10%
 Malathione: NA
Oral Ivermectin: efficacy???


URTICARIA
Definition
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
Urticaria and Angioedema
Urticaria
Angioedema
PATHOGENESIS
 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.
CLASSIFICATION
classification
According to
duration of disease
According to
clinical features
DURATION OF DISEASE

Acute urticaria




Chronic urticaria




≤ 06 weeks
Cause can be found in in approx. 50%; by history
Good prognosis
≥ 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.
ORDINARY URTICARIA
 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
Acute ordinary urticaria: ≤ 6 weeks.
Types
Allergic
Non-allergic
ALLERGIC URTICARIA (IgE mediated)

A reaction B/W an
allergen with specific
IgE antibody bound to
mast cell
 Common in atopic
persons with raised
IgE levels
Substances causing urticaria






Penicillin
Cephalosporin
Insulin
vaccines
Blood products
Bee and wasp strings
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 urticaria

Drugs






Aspirin, Other NSAIDs
Polymyxin, ciproxin, rifampsin ,vancomycin.
Radio contrast media
Plasma expanders
General anaesthetic agents
Infections
 Epstein bar virus, Hepatitis B virus
 Strept. sore throat in children
Etiology: D/B Acute VS Chronic

Acute Urticaria

Drugs

Foods
Chronic Urticaria

Physical factors
–Cold, heat, solar, pressure

Ch. Viral, bacterial, fungal infect

chronic yeast infection

autoimmune: SLE, DLE, DM, SS

Food additives

Viral: Hep: A, B, C, EBV

Insect bites and stings

Complement deficiency

Animal dander and latex

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 exam
 Skin
 Eyes
 Ears
 Throat
 Lymph nodes
 Feet
 Lungs
 Joints
 Abdomen
Lab: Assessment for
Chronic Urticaria
Initial tests
 CBC with differential
 ESR
 Urinalysis

Tests for selected patients






Stool exam. for ova, parasites, giardia
Blood chemistry profile
Antinuclear antibody titer (ANA)  Complement studies: CH50
 Cryoproteins
Hepatitis B and C
Skin prick tests (IgE-reactions)  T3, T4, TSH, Thyroid
antibodies
RAST for specific IgE
Treatment:
Pharmacologic Options

Antihistamines, others
 First-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
Corticosteroids
 Severe acute urticaria
–avoid long-term use
–use alternate-day regimen
when possible
 Avoid in chronic urticaria
(lowest dose plus antihistamines
might be necessary)
Miscellaneous
 PUVA
 Hydroxychloroquine
 Thyroxine
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 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
THANK YOU
Superior doctors prevent the disease
Mediocre doctors treat the disease before evident
Inferior doctors treat the full-blown disease
Huang Dee Nai-Chan. 2600 BC; 1st Chinese Medical Text
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