Skin disorders

Presented By:
Dr. Sally Mohamed Abd El-monem
Assistant professor of Physiology
 Introduction
Skin diseases are common and diverse, ranging from
irritating acne to life-threatening melanoma. Many are
intrinsic to the skin, but some are manifestations of diseases
involving many tissues, such as systemic lupus
erythematosus or genetic syndromes such as
neurofibromatosis.
 In this sense, the skin is a uniquely accessible “window”
through which numerous disorders can be viewed and
recognized.
 Terms for Macroscopic skin Lesions
 Excoriation: Traumatic lesion breaking the epidermis and causing a red linear mark
(i.e., a deep scratch).
 Lichenification: Thickened and rough skin characterized by prominent skin markings;
usually the result of repeated rubbing
 Macule: Flat, circumscribed area, 5 mm or less in diameter, distinguished from
surrounding skin by coloration. If greater than 5 mm, referred to as a patch.
 Papule: Elevated dome- or flat-topped lesion 5 mm or less in diameter. If greater than 5
mm in diameter, referred to as a nodule.
 Plaque: Elevated flat-topped lesion, usually greater than 5 mm in diameter.
 Pustule: Discrete, pus-filled raised lesion.
 Scale: Dry, horny, plate like excrescence;
 Vesicle: Fluid-filled raised area 5 mm or less in diameter. If greater than 5 mm in
diameter, referred to as a bulla.
 Blister is common term for both vesicles and bullae.
Terms for Macroscopic skin Lesions
Terms for Macroscopic skin Lesions
 Dermatoses
Dermatosis is a common term used for any skin disorder.
Dermatosis may be of various types such as gene tic,
inflammatory, infectious, granulomatous, connective tissue,
bullous and scaling type.
 NON-INFECTIOUS INFLAMMATORY DERMATOSES:
A very large number of skin diseases have acute or chronic
inflammation as a prominent feature.
In general, acute lesions last from days to weeks and are
characterized by inflammation (often marked by mononuclear
cells rather than neutrophils. Some acute lesions may persist,
resulting in transition to a chronic phase.
 Urticaria
is the presence of transient, recurrent,
pruritic plaques (i.e. raised
erythematous areas of oedema).
 mediated by localized mast cell
degranulation, which leads to dermal
microvascular hyperpermeability. The
resulting erythematous, edematous,
and pruritic plaques are termed
wheals.
 Pathogenesis of urticaria
In most cases, urticaria stems from an immediate (type 1)
hypersensitivity reaction.
The cause (antigen): pollens, foods, drugs (as antibiotics
and opiates), and insect venom.
The antigen → binds to immunoglobulin E (IgE)
antibodies displayed on the mast cell surface → mast
cell degranulation → dermal microvascular
hyperpermeability.
Angioedema is an uncommon variant of urticaria
 Features ( histologic and clinical)
Clinical Features:
Urticaria typically affects persons between 20 and
40 years of age, but no age is immune.
Individual lesions usually develop and fade within
hours, but episodes can persist for days or even
months
Lesions range in size and nature from small,
pruritic papules to large, edematous, erythematous
plaques.
Lesions can be confined to a particular part of the
body or generalized.
Most cases are treated with antihistamines.
Systemic steroids are used in more severe
refractory cases.
 Acute Eczematous Dermatitis (Eczema)
Eczema is a clinical term that includes
a number of conditions with variable
etiologies.
lesions take the form of red papules,
often with overlying vesicles, which
ooze and become crusted.
With persistence, these lesions develop
into raised, scaling plaques. The nature
and degree of these changes vary
among the clinical subtypes.
 The clinical subtypes of eczema
 Allergic contact dermatitis, from topical exposure to an allergen
Atopic dermatitis, now thought to stem from defects in
keratinocyte barrier function, many with a genetic basis.
Drug-related eczematous dermatitis, a hypersensitivity reaction
to a drug
Photoeczematous dermatitis, in which eczema appears as an
abnormal reaction to UV or visible light
Primary irritant dermatitis, which results from exposure to
substances that chemically, physically, or mechanically damage
the skin
 Pathophysiology of contact dermatitis
Only the most common form is contact dermatitis.
It occurs as a result of delayed (type 4 ) hypersensitivity reactions
as follows.
On first exposure to an allergen→ it penetrates the stratum
cornium→ taken by Langerhans cells → processed inside the
cells and presented on its surface → Langerhans cells migrate to
lymphnodes → the antigen reacts with T lymphocytes in L.N →
proliferation of ag specific Tcells → specific lymphocytes travel
through blood to skin.
On second exposure, the antigen reacts with t lymphocytes →
cytokine mediated inflammatory process.
 clinical features

Lesions of acute eczematous dermatitis are

pruritic (itchy), edematous, oozing plaques, often
containing vesicles and bullae. With persistent
antigen exposure,
lesions may become progressively scaly
(hyperkeratotic) as the epidermis thickens
(acanthosis). Some changes are produced or
exacerbated by scratching or rubbing of the lesion
.