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    Pathophysiology PUD

    Uploaded by

    Leah Gordoncillo
    The document discusses the pathophysiology of peptic ulcers. It notes that damage to the mucosal wall from alcohol abuse, smoking, and NSAID use can cause acid and pepsinogen release through chronic vagal response to stress. Infection with Helicobacter pylori also damages the mucosal barrier. This leads to an imbalance of aggressive and defensive factors, low mucosal and mucous cells, and loose tight junctions between cells. Infection increases gastrin and decreases somatostatin, causing erosive gastritis and decreased acid and intrinsic factor. Ultimately, the damaged mucosa cannot secrete enough mucus, leading to mucosal ulceration, possible bleeding, sc

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    Pathophysiology PUD

    Uploaded by

    Leah Gordoncillo
    3K views8 pages
    The document discusses the pathophysiology of peptic ulcers. It notes that damage to the mucosal wall from alcohol abuse, smoking, and NSAID use can cause acid and pepsinogen release through chronic vagal response to stress. Infection with Helicobacter pylori also damages the mucosal barrier. This leads to an imbalance of aggressive and defensive factors, low mucosal and mucous cells, and loose tight junctions between cells. Infection increases gastrin and decreases somatostatin, causing erosive gastritis and decreased acid and intrinsic factor. Ultimately, the damaged mucosa cannot secrete enough mucus, leading to mucosal ulceration, possible bleeding, sc

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    The document discusses the pathophysiology of peptic ulcers. It notes that damage to the mucosal wall from alcohol abuse, smoking, and NSAID use can cause acid and pepsinogen release through chronic vagal response to stress. Infection with Helicobacter pylori also damages the mucosal barrier. This leads to an imbalance of aggressive and defensive factors, low mucosal and mucous cells, and loose tight junctions between cells. Infection increases gastrin and decreases somatostatin, causing erosive gastritis and decreased acid and intrinsic factor. Ultimately, the damaged mucosa cannot secrete enough mucus, leading to mucosal ulceration, possible bleeding, sc

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    3K views8 pages

    Pathophysiology PUD

    Uploaded by

    Leah Gordoncillo
    The document discusses the pathophysiology of peptic ulcers. It notes that damage to the mucosal wall from alcohol abuse, smoking, and NSAID use can cause acid and pepsinogen release through chronic vagal response to stress. Infection with Helicobacter pylori also damages the mucosal barrier. This leads to an imbalance of aggressive and defensive factors, low mucosal and mucous cells, and loose tight junctions between cells. Infection increases gastrin and decreases somatostatin, causing erosive gastritis and decreased acid and intrinsic factor. Ultimately, the damaged mucosa cannot secrete enough mucus, leading to mucosal ulceration, possible bleeding, sc

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    of 8

    GORDONCILLO, LEAH A.

    BSN 4D Area: 3B BOOK BASE PATHOPYSIOLOGY

    CI: Sir Lourdevick Poquiz PATHOPHYSIOLOGY

    Damage to mucosal wall alcohol abuse, smoking, use of NSAIDs

    Acid and pepsinogen release with chronic vagal response to increased stress

    Infection with Helicobacter Pylori

    Damage mucosal barrier

    Imbalance of aggressive and defensive factor

    Low of mucosal cells; low quality of mucous; less of tight junction between cells

    Infection gives increased gastrin and decrease somatostatin production

    GORDONCILLO, LEAH A. BSN 4D Area: 3B

    CI: Sir Lourdevick Poquiz

    Erosive gastritis inflammation >> decrease acid and intrinsic factor

    Mucosal ulceration, possible bleeding and scaring

    Damage mucosa could not secrete enough mucus to act

    Severe Ulceration Signs and Symptoms: Epigastric pain Hematemesis/Melena Dyspepsia Pyrosis

    GORDONCILLO, LEAH A. CI: Sir Lourdevick Poquiz BSN 4D Area: 3B PATIENT BASE PATHOPHYSIOLOGY

    MODIFIABLE: Use of NSAIDs and response to increased stress

    Acid and Pepsinogen release

    Damage mucosal wall

    Imbalance of aggressive and defensive factor

    Low of mucosal cells; low quality of mucous; less of tight junction between cells

    Infection gives increased gastrin and decreased somatostatin production

    GORDONCILLO, LEAH A. BSN 4D Area: 3B

    CI: Sir Lourdevick Poquiz

    Erosive gastritis inflammation >> decreased acid and intrinsic factor

    Mucosal ulceration, possible bleeding and scaring

    A damaged mucosa could not secrete enough mucus to act as a barrier against gastric acid

    SEVERE ULCERATION Signs and Symptoms: Epigastric pain Melena Dyspepsia Pyrosis

    GORDONCILLO, LEAH A. BSN 4D Area: 3B

    CI: Sir Lourdevick Poquiz

    PATHOPHYSIOLOGY
    Predisposing Factors Factors Precipitating

    Age (40-60) >NSAIDs Gender Gastric Hyperacidity > Stress >

    Familial tendency Foods

    > Irritating

    GORDONCILLO, LEAH A. BSN 4D Area: 3B

    CI: Sir Lourdevick Poquiz

    GORDONCILLO, LEAH A. BSN 4D Area: 3B

    CI: Sir Lourdevick Poquiz

    GORDONCILLO, LEAH A. BSN 4D Area: 3B

    CI: Sir Lourdevick Poquiz

    SCHEDULE OF ACTIVTIES
    2:45 3:00 pm 3:00 3:30 pm 3:30 4:00 pm Checking of Attendance and Paraphernalia an d Assigning of patients Endorsement and Rounds Browsing of the Chart, Preparation of medicat ions and starting the Nursing care Vital Signs monitoring, Giving of medications Plotting the V/S in the TPR Nursing Care

    4:00 5:00 pm

    5:00 6:00 pm

    6:00 6:30 pm

    Feeding the patient

    6:30 - 7:30 pm

    Break time

    7:30 8:30 pm

    Vital Signs monitoring, Giving of Medications, Finalization of Nursing care I and O monitoring, Accomplishing the TPR sh eet and the chart Rechecking of the Nursing Care Plan and the Chart by our clinical instructor Endorsement Post conference followed by dismissal

    8:30 9:30 pm 9:30 10:00 pm 10:00 10:30 pm 10:30 11:00 pm

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