GI Motility Flashcards
Gastroparesis
Slow emptying of the stomach/ paralysis of the stomach -20% Type 1 diabetic patients (some type 2) Cause: Damage to the Vagus N. - Idopathic - High blood glucose (diabetic gastroparesis) Symptoms: - Nausea - Vomiting - Early feeling of fullness when eating - Weight Loss - Abdominal Bloating - Abdominal Discomfort
- DAMAGE TO THE VAGUS N IS ASSOCIATED WITH HIGH LEVELS OF GLUCOSE
Pernicious Anemia
What is it?
What causes it? (2)
Stomach does not produce enough IF
loss of Vitamin B12
Common Causes:
- Atrophic Gastritis - chronic inflammation of the stomach mucosa that leads to the loss of parietal cells
- Autoimmune Metaplastic Atrophic Gastritis - immune system attacks IF protein or gastric parietal cells
Zollinger-Ellison Syndrome
- The highest rates of H+ secretion
- A tumor (usually In the pancreas) secretes large quantities of gastrin
- Two effects of high gastrin:
1. Increased H+ secretion by parietal cells
2. Increased parietal cell mass - The delivery of excessive amounts of H+ to the duodenum overwhelms the buffering capacity of the duodenum. - Overwhelms the buffering capacity of HCO3- in pancreatic juices and erodes the mucosa and produces an ulcer
- Can cause STEATORRHEA - low duodenal pH will inactivate the pancreatic lipases necessary for fat digestion
Secretin stimulation test
Peptic Ulcers
- Caused by H. pylori infection and the use of NSAIDs (Asprin)
- Ulcerative lesion of gastric or duodenal mucosa
- Cause by the erosive and digestive action of H+ and pepsin on the mucosa which is normally protected by the layer of mucus and HCO3-
- Could be the result of:
- Loss of protective mucosal barrier
- Excessive H+ and pepsin secretions
- Combination of the two
Two types: gastric ulcers and duodenal ulcers
Gastric Ulcers
Found in the lining of the stomach - main problem is the defective gastric mucosa barrier, rather than having an increase in acid production.
Net H+ is LOWER because some of the secreted H+ leaks into the damaged mucosa –> secretion of gastrin is INCREASED because of the reduced net H+
Major causative agent is H. pylori
Duodenal Ulcers
- Formed on the lining of the duodenum
- More common than gastric ulcers
- Usually do not become malignant
- H+ secretion is HIGHER than normal –> if excess H+ is delivered to the duodenum then it will overwhelm the buffering capacity of HCO3- in pancreatic juice
Acting with pepsin, this excess H+ will digest and damage the duodenal mucosa - Caused by H. pylori infection