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  • Pathophysiology Scleroderma

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    Suzette Pipo
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    The document outlines several modifiable and non-modifiable factors that can contribute to the development of systemic sclerosis or scleroderma. Non-modifiable factors include gender, age, and genetic makeup. Modifiable factors include environmental triggers, hormones, infections, drugs, UV radiation, and vascular injury. If left unaddressed, these modifiable factors can lead to endothelial cell dysfunction, abnormal constriction of blood vessels, tissue hypoxia, and fibrosis of the skin and internal organs. Common clinical manifestations involve the esophagus, stomach, skin, and other organs.

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    Scleroderma

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    The document outlines several modifiable and non-modifiable factors that can contribute to the development of systemic sclerosis or scleroderma. Non-modifiable factors include gender, age, and genetic makeup. Modifiable factors include environmental triggers, hormones, infections, drugs, UV radiation, and vascular injury. If left unaddressed, these modifiable factors can lead to endothelial cell dysfunction, abnormal constriction of blood vessels, tissue hypoxia, and fibrosis of the skin and internal organs. Common clinical manifestations involve the esophagus, stomach, skin, and other organs.

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    © All Rights Reserved
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    123 views1 page

    Pathophysiology Scleroderma

    Uploaded by

    Suzette Pipo
    The document outlines several modifiable and non-modifiable factors that can contribute to the development of systemic sclerosis or scleroderma. Non-modifiable factors include gender, age, and genetic makeup. Modifiable factors include environmental triggers, hormones, infections, drugs, UV radiation, and vascular injury. If left unaddressed, these modifiable factors can lead to endothelial cell dysfunction, abnormal constriction of blood vessels, tissue hypoxia, and fibrosis of the skin and internal organs. Common clinical manifestations involve the esophagus, stomach, skin, and other organs.

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    © All Rights Reserved
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    cvcc

    Non Modifiable:
    Gender: Female
    Age
    Genetic Makeup


    Modifiable:
    Environmental triggers
    Hormones
    Infections(Viruses &bacteria)
    Drugs
    UV radiation
    Vascular Injury
    Abnormal Constriction of Blood Vessels
    Overgrowth of endothelial & muscle cells of Blood vessels
    Endothelial cells dysfunction and activation
    Vasoactive mediators
    The ability of endothelial cells
    realease of Prostacyclin is reduced
    Production and responsiveness of
    Endothlin 1 to vasodilatory factor is
    defective
    Hypertrophy of intimal& medial
    layers of blood vessels along with
    fibrosis results in luminal fibrosis
    Vasculopathy
    Tissue hypoxia
    Platelet activation
    Fibroblast activation
    Overproduction of Collagen &fibronectin in dermis
    Fibrosis in Skin & organs
    Epidermal atrophy
    Calcium Calm, hardening of
    the fascia muscle atrophy
    Smooth muscle is undergoing homogenous sclerosis atrophy & fibrosis
    Low lower esophagealsphincter(LES) pressure
    & failure of the LES to relax

    GERD occurs
    Esophagealinjury
    dysphagia,
    odynophagia,
    heartburn and
    regurgitation.
    Calcinosis
    Sclerodactyl
    Raynauds phenomenon
    Gastric involvement
    Delayed gastric emptying, or
    gastroparesis, is the most
    common gastric manifestation
    leading to nausea, vomiting and
    postprandial fullness
    Gastritis
    Colchicine
    Prednisone



    Pirsec
    penicillamine
    Rosuvastatin

    Kailiumdurule
    PATHOPHYSIOLOGY

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