This document outlines the pathophysiological process that leads to appendicitis. It begins with constipation and a low fiber diet, which can cause a fecalith to block the appendix. This blockage decreases drainage from the appendix and increases pressure, reducing blood flow and oxygen supply. As a result, the appendix becomes necrotic and vulnerable to bacterial invasion, triggering an inflammatory response. Symptoms include nausea, vomiting, abdominal pain, and risk of infection if the appendix ruptures. Ultimately, appendicitis requires an appendectomy, further exacerbating the inflammatory response and causing postsurgical pain and healing.
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pathophysiology-of-appendicitis
1. Episodes of Constipation Low Fiber Diet
↓ ↓
↓
Occlusion of Appendix by Fecalith
↓
Decreased flow/drainage of mucosal secetions
↓
Increased ILP in the appendix
↓
Vasocongestion
↓
Decreased blood supply in the appendix
↓
Decreased O2 supply in the appendix
↓
Appendix starts to be necrotic; Bacteria invade the appendix
↓
Disruption of Cell Membrane of Appendix
↓
Start of Inflammatory Process
↓
↓ ↓ ↓
Release of Chemical Mediators Activation of the Vomiting Neutrophils to area
Center in the Medulla
↓ ↓
---> Histamine, Prostaglandin, Stimulation of Vagus Suppression of Pus Formation
Leukotrienes, Bradykinin Nerve Sympathetic (phagocytized bacteria
↓ GI Function and dead cells)
Swelling of Appendix Risk for Infection
(if appendix ruptures)
---> Prostaglandin, Bradykinin Nausea & Vomiting Anorexia
↓
Pain in the RLQ of Abdomen Risk for Deficient Risk for Imbalanced Nutrition
↓ Fluid Volume less than body requirements
Acute Pain
---> Interleukin-1
↓
Increased WBC
Inflammation of Appendix (Appendicitis) <
↓
Appendectomy
↓
Tissue Trauma
↓
Open Wound Disruption of Cell Membrane Nociceptors on the
↓ ↓ ↓ Dermis
Impaired Tissue Risk for Start of Inflammatory ↓
Integrity Infection Process Send Impulse to CNS
Release of Prostaglandin/ Pain on Surgical
Bradykinin Site
Activity Intolerance