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Disorder of eccrine sweat glands
• Present all over the body especially on the
palms, soles and in axillae.
• Multiple factors are controlling rate of
sweating-temp., hormones, emotions,
gustatory.
• Disorders:
• Generalized hyperhidrosis
• Hypo and anhidrosis
• miliaria
Miliaria
• Spillage of sweat into dermis due to obstruction and
rupture of eccrine sweat ducts.
• Occurs – hot humid climate
• Variation according to level of rupture:
• Miliaria crystallina (rupture below stratum corneum)
– Tiny clear noninflammed vesicles.
• Miliaria rubra(rupture in epidermis)
– Pricking or burning sensation with small
erythematous papules surmounted by vesicles.
• Miliaria profunda(rupture in dermoepidermal juncn.)
– Larger erythemaouts papules
treatment
•
•
•
•
Avoid humid and humid places
Avoid synthetic garments
Calamine lotion
Severe cases: short course of mild topical
steroid
Disorder of apocrine gland
• Present in axillae, nipples, periumbilical area,
perineum and genitalia.
• Duct of the gland connects into mid portion of
the hair follicle .
• Becomes functional just before puberty.
Disorder
• Hidradenitis suppurtiva (apocrine acne)
• Cause unknown
• Microbs like staph. Aureus, anaerobic strpt.
And bacteroides are often found in the lesions
but their role in the pathogenesis is doubtful
• Lesions seen are ndules, pustules, cysts and
sinuses with interconnecting bridges.
Comedones frequently seen.
• Site-axilla, groins and perianal region.
• Treatment:
• Severe cases large area of vault of axilla is excised to
remove apocrine glands to prevent recurrences.
• Medical :
– Systemic antibiotics like tetracyclines and
erythromycin)
– Systemic antiandrogen and retinoids
– Isotretinoin
– Incision and drainage
– Intralesional inj. Of triamcinolone
ABNORMAL VASCULAR RESPONSE
• Both exogenous and endogenous stimuli can trigger vascular
responses in skin.
• At the beginning the epidermis is normal and later it may
show changes in the form of necrosis mainly due to vascular
compromise.
• Different forms:
– Vascular dilatation –erythema
– Dermal and subcut. Oedema –urticaria and
angioedema
– Extravasation of blood due to vessel wall
inflammation -vasculitis
ERYTHEMA MULTIFORME
• As its name implies, this is a reaction pattern of multiform
erythematous lesions.
• PROVOKING FACTORS IN ERYTHEMA MULTIFORME
• Herpes simplex infections
• Other infections, e.g. mycoplasma ,hepatitis A,histoplasmosis
• Bacterial infections
• Drugs, especially sulphonamides, penicillins ,carbamazepine,
phenitoin and barbiturates (most frequent in SJS-TEN
COMPLEX)
• Internal malignancy or its treatment with radiotherapy
• SLE,graft vs host rxn.,lymphoreticular malignancies
• Idiopathic (5%)
• The multiform erythematous lesions may be urticaria-like and
some have obvious 'bull's-eye' or 'target' lesions.
• Blisters may be seen in the centre or around the edges of the
lesions
• In some cases blisters dominate the picture; the StevensJohnson syndrome-toxic epidermal necrolysis comples(SJSTEN complex) is severe bullous erythema multiforme with
emphasis on mucosal involvement including the mouth, eyes
and genitals, with constitutional disturbance.
• Oral mucosa: hemorrhagic crusting of lips. Bullae which
rapidly rupture to form erosions covered with grayish white
slough
• Eyes: purulent conjunctivitis, corneal erosions
• Genital mucosa: erosion s and complicated by urinary
retention
• Nasal mucosa: erosions
• SJS-TEN complex is clinically graded into
• SJS- when the body surface area involves<10%
• SJS-TEN- when BSA 10-30%
• TEN- >30%
• Management
• Usually no treatment is required although
symptomatic relief can be obtained with
simple dressings.
• Stevens-Johnson syndrome can be treated
with a short course of intravenous
immunoglobulin. Corticosteroids are best
avoided.
ERYTHEMA NODOSUM
• This characteristic reaction pattern is due to a vasculitis in the
deep dermis and subcutaneous fat.
• Clinical features
• Painful, palpable, dusky blue-red nodules
• most commonly seen on the lower legs.
• Malaise, fever and joint pains are common.
• The lesions resolve slowly over a month, leaving bruise-like
marks .
• PROVOKING FACTORS IN ERYTHEMA NODOSUM
• Infections •Bacteria (streptococci, tuberculosis, brucellosis
and leprosy), viruses, mycoplasma, rickettsia, chlamydia and
fungi
• Drugs •e.g. Sulphonamides and oral contraceptives
• Systemic disease •e.g. Sarcoidosis, ulcerative colitis and
Crohn's disease
• Management
• The underlying cause should be determined and treated. Bed
rest and oral NSAIDs may hasten resolution. Tapering systemic
corticosteroid courses may be required in stubborn cases.
urticaria
• Also known as hives.
• Eruption characterized by transient usually
pruritic wheals due to acute dermal oedema
from the extravascular leakage of plasma.
• Angioedema signifies larger areas of oedema
involving the dermis and subcutis.
Aetiopathogenesis
• Immune
• Non immune
• Lesion occurs due to release of biologically
active substances from mast cells particularly
histamine.
• Histamine causes vasodilatation and increased
vascular permeability.
Different pathways involved
• Antigen induced , IgE mediate histamine
release from tissue mast cells causing
immediate hypersensitivity.
• Mast cell degranulation through the classical
complement pathways.
• Direct mast cell degranulation by certain drugs
and chemicals
Preformed mediators in granules
• Histamine
bronchoconstriction, mucus secretion,
vasodilatation, vascular permeability
• Tryptase
proteolysis
• kininogenase
kinins and vasodilatation, vascular
permeability, edema
Newly formed mediators
• leukotriene B4
 basophil attractant
• leukotriene C4, D4
 same as histamine but 1000x more potent
• prostaglandins D2
 edema and pain
• PAF
 platelet aggregation and heparin release:
microthrombi
Classification of urticaria
Group
• Chronic
• Acute
• Physical
• Contact
• Pharmacological
• Systemic
• Inherited
• others
Example
• Idiopathic
• Ige mediated e.g food
allergy,drug reaction.
• Dermographism,cholinergic,
cold,solar,heat,delayed
pressure.
• Food allergans
• Aspirin ,opiates,non
streroidal drugs,
• LE,lymphoma,thyrotoxixosis
infections,
• Heriditary angioedmea.
• Insect bite ,mastocytosis.
Clinical presentation
• Common is chronic idiopathic form.
• No cause is found
• Itchy pink color wheals appear either as
papules or plaques anywhere in the skin.
• Typically they last for less than 24 hours and
dissappear without a trace .
• Wheals may be round ,annular or polycyclic
and vary in diameter from few mm to several
cm.
• Their number can vary from few to many.
• Angioedema usually with oedema of the
tongue and lips may occur.
• Resolves spontaneously within few months.
Acute form
•
•
•
•
Sudden form may be due to Ige mediated type 1 reaction.
Patients can often identify the allergens.
Commonly it is a food or a drug.
Acute urticaria is commonly caused by a variety of infections,
medications, food allergies, physical stimulants, chemicals,
chronic inflammatory diseases, and insect bites, as follows:
– Recent infection from a viral syndrome or an upper
respiratory tract illness (39%)
– Medications (eg, ACE inhibitors, aspirin, nonsteroidal
anti-inflammatory drugs, sulfa-based drugs, penicillins,
diuretics, opioids, polymyxin B)
– Food and food additives (eg, nuts, fish, shellfish, eggs,
chocolate, strawberries, salicylate, benzoates)
– Parasitic infections (eg, Ascaris, Ancylostoma,
Strongyloides, Echinococcus, Trichinella, Filaria)
– Physical stimulants (eg, cold, pressure, aquagenic)
– Chemicals (eg, latex, ammonium persulfate in hair
chemicals)
– Intravenous radiocontrast media
– Arthropod bites
wheal
Physical urticaria
• Cold ,heat sun exposure ,pressure and even
water can induce urtricaria .
• Dermographism may be found.
• Wheal in cholinergic urtricaria is itchy with
small papules that appears in response to
sweating as induced by exercise ,heat,emotion
,or spicy food.it may last for few mins to few
hours .
Dermographism
Hereditary angioedema
• Autosomal dominant.
• Usually fatal
• Episode of angioedema involving larynx and gi
tract.
• Due to defficiency of c1 esterase inhibitor that
causes the activation of complement pathway
and accumulation of vasoactive mediators.
• In acute condition fresh frozen plasma are given .
• In long term danazol is given .
Angioedema
Management
• Underlying cause should be eliminated.
• Desensitization
• Main stay of treatment is with antihistaminics.
• Cetirizine (Zyrtec)
• Second-generation antihistamine with markedly reduced
sedative effects and reduced anticholinergic effects. Forms
complex with histamine for H1 receptor sites in blood
vessels, GI tract, and respiratory tract.
• Adult
• 5-10 mg PO
• Fexofenadine (Allegra)
• Competes with histamine for H1 receptors on GI tract,
blood vessels, and respiratory tract, reducing
hypersensitivity reactions. Does not sedate.
• SR: 180 mg PO
Histamine H2 antagonists
• Cimetidine (Tagamet)
• H2 antagonist that when combined with an H1
antagonist may be useful in treating itching
and flushing in urticaria and contact
dermatitis that do not respond to H1
antagonists alone. Use in addition to H1
antihistamines.
• 300 mg PO qid
• Corticosteroid:used occassionaly in severe cases
and in angioedema and urticarial vasculitis.
Prednisone
• Immunosuppressant for treatment of
autoimmune disorders; may decrease
inflammation by reversing increased capillary
permeability .Stabilizes lysosomal membranes
and suppresses lymphocytes and antibody
production.
• 0.5-2 mg/kg/d PO; taper as condition improves;
single morning dose is safer for long-term use,
but divided doses have more anti-inflammatory
effect
Adrenaline
• Acute airway obstruction or anaphylactic
shock
• Adrenaline together with an antihistaminics
chlorpheniramine should be given i.v slowly.
• Adrenaline dose 0.5-1 mg 0.5-1 ml of 1/1000.