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    integumentary system

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    integumentary system

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    Integumentary system

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    Integumentary system

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    Download as docx, pdf, or txt
    3 views10 pages

    integumentary system

    Uploaded by

    aslamshaista85
    Integumentary system

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    © All Rights Reserved
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    Skin Lesions

    Skin lesions are abnormal changes in the skin’s texture, color, or shape and
    can be categorized as primary or secondary:

    Primary Lesions: Direct results of a disease or condition. Examples include:

    Macules: Flat discolorations (e.g., freckles).

    Papules: Small, raised bumps (e.g., warts).

    Vesicles: Fluid-filled sacs (e.g., blisters).

    Pustules: Pus-filled lesions (e.g., acne).

    Secondary Lesions: Develop from primary lesions or external factors (e.g.,


    infection, scratching). Examples include:

    Crusts: Dried blood or pus on the skin.

    Ulcers: Open sores due to tissue loss.

    Scales: Flaking skin from conditions like psoriasis.

    Aging and the Integumentary System

    The integumentary system includes the skin, hair, nails, and glands. Aging
    affects its structure and function:

    Skin Changes:

    Thinning of the epidermis and dermis: Skin becomes more fragile and prone
    to injury.

    Loss of elasticity: Reduced collagen and elastin lead to wrinkles and sagging.

    Decreased melanin production: Causes uneven pigmentation and age spots.

    Reduced barrier function: Increased risk of infection and dehydration.

    Hair and Nail Changes:

    Hair grays and thins due to decreased melanin.

    Nails grow slower and may become brittle.

    Glandular Changes:

    Sebaceous glands produce less oil, leading to dry skin.

    Sweat glands become less active, impairing temperature regulation.


    Signs and Symptoms of Skin Diseases

    Common signs and symptoms that may indicate a skin condition include:

     Discoloration: Redness, dark spots, or loss of pigmentation (e.g.,


    vitiligo).
     Texture Changes: Scaliness, roughness, or thickened skin.
     Itching or Pain: Common in conditions like eczema, psoriasis, or
    shingles.
     Lesions or Rashes: May present as bumps, pustules, blisters, or
    patches.
     Swelling or Inflammation: Often indicates an allergic reaction or
    infection.
     Cracking or Peeling Skin: Seen in dryness or fungal infections.
     Excessive Hair Loss or Growth: May indicate hormonal imbalances or
    autoimmune conditions.

    Common Examples

    Eczema: Red, itchy, dry patches often in the bends of the elbows and knees.

    Psoriasis: Thick, silvery scales on the scalp, elbows, or knees.

    Acne: Blackheads, whiteheads, or inflamed pustules on the face, chest, or


    back.

    Shingles: Painful rash with blisters, often on one side of the body.

    Skin infections
    Bacterial, viral and fungal infections
    Impetigo

     Definition: A superficial bacterial skin infection caused by


    Staphylococcus aureus or Streptococcus pyogenes.
     Pathogenesis:
    o Bacterial invasion through minor skin breaks.
    o Toxin production (e.g., exfoliative toxins in staphylococcal
    impetigo).
     Morphological Features:
    o Intraepidermal pustules.
    o Subcorneal vesicles filled with neutrophils.
     Clinical Features:
    o Honey-colored crusts over erythematous bases, especially on the
    face and extremities.
    o Contagious and common in children.

    Tinea (Dermatophytosis)

     Definition: Fungal infection of keratinized tissue caused by


    dermatophytes (Trichophyton, Microsporum, Epidermophyton).
     Pathogenesis:
    o Fungi invade keratinized structures (stratum corneum, nails, and
    hair).
    o Elicit a mild inflammatory response.
     Morphological Features:
    o Fungal hyphae in the stratum corneum.
    o Hyperkeratosis and mild spongiosis.
     Clinical Features:
    o Scaly, annular plaques with central clearing ("ringworm")
    o Common forms: tinea corporis, tinea capitis, and tinea pedis.
    Herpes Simplex Virus (HSV) Infections

     Definition: Viral infection of the skin and mucosa caused by HSV-1


    (oral) and HSV-2 (genital).
     Pathogenesis:
    o Virus infects keratinocytes and establishes latency in sensory
    ganglia.
    o Reactivation occurs due to stress, trauma, or
    immunosuppression.
     Morphological Features:
    o Multinucleated giant cells.
    o Intraepidermal vesicles with ballooning degeneration of
    keratinocytes.
    o Inclusion bodies.
     Clinical Features:
    o Painful vesicles on erythematous bases.
    o Recurrent outbreaks in the same location.
    Skin disorders associated with immune system dysfunction

    1. Psoriasis
    Definition:

    A chronic autoimmune skin disorder characterized by rapid epidermal proliferation and


    inflammation.

    Pathogenesis:

     Immune dysregulation: Overactivation of T-helper cells (Th1 and


    Th17) leads to cytokine release (e.g., TNF-α, IL-17, IL-23), triggering
    keratinocyte hyperproliferation.
     Genetic predisposition (HLA-Cw6) and environmental triggers (stress,
    infection, trauma).

    Morphological Features:

     Hyperkeratosis (thickened stratum corneum), parakeratosis (retained


    nuclei in stratum corneum), and elongated rete ridges.
     Munro microabscesses (neutrophil collections in the stratum corneum)
    and spongiform pustules.

    Clinical Features:

     Well-demarcated, erythematous plaques with silvery scales, commonly


    on extensor surfaces.
     Associated with nail changes (pitting, onycholysis) and psoriatic
    arthritis in some cases.
    2. Systemic Lupus Erythematosus (SLE)
    Definition:

    A multisystem autoimmune disease with skin manifestations due to immune complex deposition.

    Pathogenesis:

     Autoantibodies (e.g., ANA, anti-dsDNA) form immune complexes


    that deposit in skin and other organs, leading to inflammation via
    complement activation.
     Environmental triggers (UV radiation, infections) exacerbate the
    disease in genetically predisposed individuals.

    Morphological Features:

     Hydropic degeneration of basal keratinocytes.


     Thickened basement membrane.
     Lymphocytic infiltrates at the dermo-epidermal junction.

    Clinical Features:

     Acute cutaneous lupus: Malar rash ("butterfly rash") following sun


    exposure.
     Chronic cutaneous lupus (Discoid lupus): Well-defined, scaly
    plaques on the scalp, face, or ears, with scarring and pigment changes.
    3. Atopic Dermatitis (Eczema)
    Definition:

    A chronic inflammatory skin condition characterized by pruritus and eczematous lesions.

    Pathogenesis:

     Dysregulated immune response with predominance of Th2 cytokines


    (IL-4, IL-13) leading to impaired skin barrier (filaggrin gene mutation).
     Increased IgE levels and susceptibility to allergens and microbes.

    Morphological Features:

     Spongiosis (intercellular edema in the epidermis).


     Lymphocytic infiltrates in the dermis.
     Hyperkeratosis in chronic stages.

    Clinical Features:

     Pruritic, erythematous, oozing papules and plaques, often on flexural


    areas (e.g., antecubital and popliteal fossae).
     Associated with allergic rhinitis and asthma (atopic triad).

    4. Pemphigus Vulgaris
    Definition:

    A life-threatening autoimmune blistering disorder caused by loss of intercellular adhesion.


    Pathogenesis:

     Autoantibodies against desmoglein 1 and 3 in desmosomes disrupt


    keratinocyte adhesion (acantholysis).
     Often associated with HLA-DR4 and environmental factors (e.g., drugs).

    Morphological Features:

     Suprabasal acantholysis forming intraepidermal bullae.


     Row of tombstone appearance of basal keratinocytes.

    Clinical Features:

     Flaccid bullae that rupture easily, leaving erosions.


     Nikolsky's sign positive (skin shears off with pressure).
     Commonly affects mucosa (e.g., oral cavity).

    5. Bullous Pemphigoid
    Definition:

    An autoimmune blistering disorder characterized by subepidermal bullae.

    Pathogenesis:

     Autoantibodies against hemidesmosomal proteins (BP180 and


    BP230) in the basement membrane zone.
     Complement activation leads to dermal-epidermal separation.

    Morphological Features:

     Subepidermal blisters filled with eosinophils and neutrophils.


     Linear deposition of IgG and C3 along the basement membrane
    (immunofluorescence).

    Clinical Features:

     Tense, fluid-filled bullae on erythematous or normal skin.


     Commonly affects elderly individuals and spares mucosa.
    6. Vitiligo
    Definition:

    An autoimmune disorder causing depigmentation due to melanocyte destruction.

    Pathogenesis:

     Cytotoxic T-cell-mediated destruction of melanocytes.


     Genetic predisposition and environmental triggers (e.g., trauma,
    sunburn).

    Morphological Features:

     Loss of melanocytes in affected areas.


     Absence of melanin pigment in histological sections.

    Clinical Features:

     Well-demarcated depigmented macules and patches, often


    symmetrically distributed.
     Frequently involves face, hands, and genital areas.

    7. Scleroderma (Systemic Sclerosis)


    Definition:

    A chronic autoimmune disorder characterized by excessive fibrosis of skin and internal organs.

    Pathogenesis:

     Overproduction of collagen due to fibroblast activation, driven by


    cytokines (e.g., TGF-β).
     Microvascular damage contributes to ischemia and fibrosis.

    Morphological Features:

     Dermal fibrosis with loss of adnexal structures.


     Thickened collagen bundles.

    Clinical Features:

     Limited type (CREST syndrome): Calcinosis, Raynaud phenomenon,


    Esophageal dysmotility, Sclerodactyly, and Telangiectasia.
     Diffuse type: Widespread skin thickening with organ involvement
    (lungs, heart, kidneys).

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