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    Patophy of Pud

    Uploaded by

    Clarence Bravio
    This document provides a schematic overview of the pathophysiology of peptic ulcers. It lists contributing factors like diet, alcohol, smoking, and genetics. Precipitating factors include age over 50, low socioeconomic status, H. pylori infection, and NSAID use. Excess stomach acid and H. pylori infection can damage the stomach lining, impairing its protective mechanisms. This allows acid to further erode the mucosa, potentially causing ulcers, bleeding, and other symptoms like epigastric pain or dyspepsia. Advanced cases can lead to hematemesis, melena, or hemorrhage if bleeding becomes excessive.

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    Patophy of Pud

    Uploaded by

    Clarence Bravio
    139 views4 pages
    This document provides a schematic overview of the pathophysiology of peptic ulcers. It lists contributing factors like diet, alcohol, smoking, and genetics. Precipitating factors include age over 50, low socioeconomic status, H. pylori infection, and NSAID use. Excess stomach acid and H. pylori infection can damage the stomach lining, impairing its protective mechanisms. This allows acid to further erode the mucosa, potentially causing ulcers, bleeding, and other symptoms like epigastric pain or dyspepsia. Advanced cases can lead to hematemesis, melena, or hemorrhage if bleeding becomes excessive.

    Original Description:

    Peptic ulcer disease

    Original Title

    PATOPHY OF PUD

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    This document provides a schematic overview of the pathophysiology of peptic ulcers. It lists contributing factors like diet, alcohol, smoking, and genetics. Precipitating factors include age over 50, low socioeconomic status, H. pylori infection, and NSAID use. Excess stomach acid and H. pylori infection can damage the stomach lining, impairing its protective mechanisms. This allows acid to further erode the mucosa, potentially causing ulcers, bleeding, and other symptoms like epigastric pain or dyspepsia. Advanced cases can lead to hematemesis, melena, or hemorrhage if bleeding becomes excessive.

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    139 views4 pages

    Patophy of Pud

    Uploaded by

    Clarence Bravio
    This document provides a schematic overview of the pathophysiology of peptic ulcers. It lists contributing factors like diet, alcohol, smoking, and genetics. Precipitating factors include age over 50, low socioeconomic status, H. pylori infection, and NSAID use. Excess stomach acid and H. pylori infection can damage the stomach lining, impairing its protective mechanisms. This allows acid to further erode the mucosa, potentially causing ulcers, bleeding, and other symptoms like epigastric pain or dyspepsia. Advanced cases can lead to hematemesis, melena, or hemorrhage if bleeding becomes excessive.

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    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    of 4

    SCHEMATIC PATHOPHYSIOLOGY

    Contributing Factor: Precipitating Factors:

     Diet: Excessive caffeine intake  Age: 50-70 years old


     Increase hydrochloric acid (HCL) production
     Excessive alcohol intake
     Low socioeconomic status
     Smoking
     Unclean foods and water
     Stress factors  Unsanitary living condition
     Type “0” blood  Irritation to the lining of (mucosal), proximal
     Genetic predisposition of small intestines
     Gastric acid secretion  Presence of Helicobacter Pylori infection
     Ulcerogenic substances (NSAID’s e.g aspirin,
    ibuprofen)

    Excessive production of Entry of H.pylori through


    Excessive NSAID use
    Hydrochloric acid (HCL) ingestion

    Irritation of the lining Renders the mucosa Toxicity to gastric


    (mucosal) of the stomach, more vulnerable to acid COX-1 inhibition epithelial cell
    duodenum, proximal of damage by disrupting
    small intestines mucous layer, liberating
    enzymes and adhering to
    gastric epithelium.

    Decreased
    Imbalances between prostaglandins
    protective mechanisms
    Altered gastric
    and the acid-pepsin
    secretion
    proteolytic enzymes

    Decreased gastric
    Tissue injury in the mucous production
    stomach/ Ulcers

    Can damage mucosal barrier

    Can cause activation of inflammatory process


     Decreased function of mucosal cells
     Decreased quality of mucus
     Loss of tight junction between cells

    Back diffusion of acid into gastric mucosa

    Conversion of pepsinogen to Increased acid Formation of liberation of


    pepsin secretion histamine

     Further mucosal erosion Local vasodilation


     Destruction of blood Stimulation of cholinergic
    intramural plexus, causing muscle
    spasm

    Ulceration Epigastric pain  Increased capillary permeability


     Loss of plasma proteins
     Mucosal edema
    Bleeding in Bleeding in  Loss of plasma into gastric lumen
    Dyspepisia
    esophagus stomach

    Excessive
    bleeding
    Hematemesis (hemorrhage)
    (Vomiting of
    blood)
    Blood passes through GI
    Decreased oxygen tract becomes oxidized by
    carrying capacity as HCl resulting in
    manifested by
    Blood gets decreased hgb and *Black tarry stool Pyloric
    oxidized by hct level obstruction
    HCl but
    moves back
    to esophagus
     Pallor
     Lightheadedness
    Coffee-ground  Weakness
    emesis

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