Pa Tho Physiology Of Acute Gastroenteritis

PATHOPHYSIOLOGY OF ACUTE GASTROENTERITIS Ingestion of fecally contaminated food & water Direct invasion of the bowel wall

Endotoxins are released Stimulation and destruction of mucosal lining of the bowel wall

Pain ulceration

Attempted defecation (tenesmus)

bleeding

hematochezia

Digestive & absorptive malfunction

melena

hematemesis Nausea & vomiting

Excessive gas formation GI distention Flatus Secretion of F&E in the intestinal lumen

Increase secretion of Cl & HCO3 ions in the bowel Increase peristaltic movement

Hyperactive bowel sound (borborygmi)

Mild diarrhea (2-3 stools)

Inhibition of Na reabsorption

F&E imbalance

hypernatremia Increase protein in the lumen

LI is overwhelmed & unable to reabsorb the lost fluid Intense diarrhea (>10x) (watery stool) Serious fluid volume deficit Hypotension

Hypovolemic shock

Death

Metabolic acidosis

Kussmauls breathing

Acute gastroenteritis is usually caused by bacteria and protozoan. In the Philippines, one of the most common causes of acute gastroenteritis is E. histolytica. The pathologic process starts with ingestion of fecally contaminated food and water. The organism affects the body through direct invasion and by endotoxin being released by the organism. Through these two processes the bowel mucosal lining is stimulated and destroyed the eventually lead to attempted defecation or tenesmus as the body tries to get rid of the foreign organism in the stomach. The client with acute gastroenteritis may also report excessive gas formation that may leads to abdominal distention and passing of flatus due to digestive and absorptive malfunction in the system. Feeling of fullness and the increase motility of the gastrointestinal tract may progress to nausea and vomiting and increasing frequency of defecation. Abdominal pain and feeling of fullness maybe relieved only when the patient is able to pass a flatus. As the destruction of the bowel continues the mucosal lining erodes due to toxin, direct invasion of the organism and the action of the hydrochloric acid of the stomach. As the protective coating of the stomach erodes the digestive capabilities of the acid helps in destroying the stomach lining. Pain or tenderness of the abdomen is then felt by the patient. When the burrows or ulceration reaches the blood vessels in the stomach bleeding will be induced. Dysentery may be characterized by melena or hematochezia depending on the site and quantity of bleeding that may ensue. Signs of bleeding may be observed also through hematemesis. As the bowel is stimulated by the organism and its toxin, the intestinal tract secretes water and electrolytes in the intestinal lumen. The body secretes and therefore lost Chloride and bicarbonate ions in the bowel as the body try to get rid of the organism by increasing peristalsis and number of defecation. Sodium and water reabsorption in the bowel is inhibited with the lost of the two electrolytes. Mild diarrhea is characterized by 2-3 stool, borborygmi (hyperactive bowel sound),fluid and electrolyte imbalance and hypernatremia. When the condition continue to progress, protein in the body is excreted to the lumen that further decreases the reabsorption and the body become overwhelmed that leads to intense diarrhea with more than 10 watery stool. Serious fluid volume deficit may lead to hypovolemic shock and eventually death.