I. Pathogenesis.
Pyloric obstruction can be caused by local inflammatory edema of the ulcer or by spasm of the pyloric sphincter, or by scarring formed during repair of the ulcer. These two factors can coexist, but mostly one factor is dominant.
II. Pathogenesis.
1, pathological typing.
Gastric pyloric obstruction is divided into 3 types.
① reflex spasm of the pyloric sphincter, and the obstruction is intermittent.
(ii) pyloric obstruction is edematous and also manifests as intermittent.
(iii) scarring, which is persistent and is an absolute indication for surgery. In the initial stage of obstruction, the gastric wall thickens compensatingly by enhancing peristalsis to promote emptying.
2.Pathophysiology.
Once the obstruction occurs, food and gastric juice are retained and cannot enter the small intestine through the pylorus, and even vomiting occurs, which not only affects the digestion and absorption of normal food, but also causes abnormal loss of large amount of water and electrolytes, thus causing a series of pathophysiological changes in the whole body and local area.
(1) Systemic pathophysiological changes.
(1) Nutritional disorders: Insufficient digestion and absorption of ingested food, coupled with vomiting, will inevitably lead to nutritional disorders, including anemia and hypoproteinemia, etc.
②Disorders of water and electrolytes: normal adults secrete 1500ml of saliva and 2500ml of gastric juice per day, totaling about 4000ml. When the pylorus is obstructed, the secreted fluid is not absorbed, but the electrolytes are lost due to vomiting. The loss of water first affects the extracellular fluid, as a result, the osmotic pressure of the extracellular fluid increases and the intracellular water moves out, causing intracellular dehydration. If vomiting continues and is not replenished, circulatory failure may occur.
Since vomit still contains a large amount of electrolytes, the following conditions can occur.
1. Potassium deficiency: Since the potassium content in gastric juice is higher than that of serum potassium, potassium ions can be lost in large quantities when gastric juice is lost in large quantities, plus the patient cannot eat and cannot obtain it from food, and the kidneys continue to excrete potassium, which can make potassium even more deficient. In the state of starvation, catabolism occurs in the body, as a result, potassium is moved from intracellular to extracellular, and at this time, although there is a heavy potassium deficiency, serum potassium can be only slightly below normal, which is easily misdiagnosed.
2, sodium deficiency: although the content of sodium in gastric juice is lower than plasma, but if a large amount of vomiting, and can not be ingested through the mouth, can also cause sodium deficiency. In patients with pyloric obstruction, due to massive vomiting, extracellular fluid is reduced and blood is concentrated, so plasma sodium is only mildly reduced, which is also easy to be misdiagnosed.
3, acid-base balance disorder: normal gastric wall cells can make water and CO2 to generate carbonic acid, the latter dissociated into H+ and HCO3-, H+ into the lumen of the glandular duct and Cl- combined into hydrochloric acid (HCl), HCO3- is back to the circulation. The intestinal mucosa epithelium can also produce carbonic acid (H2C03) in an alkaline environment, which dissociates into HCO2- and H+, the former entering the intestinal fluid and the latter returning to the blood circulation to be neutralized with HC03- in the blood circulation; the HCl in the gastric fluid is neutralized with HC03- in the intestine, thus achieving acid-base balance. In the case of pyloric obstruction, the above balance is disrupted due to the massive loss of HCl in the stomach due to massive vomiting, which gradually increases the HCO3- in the blood and destroys the ratio of (HCO3-)/(H2CO3), resulting in an increase in the total amount of buffered bases in the blood and a rise in pH, causing metabolic alkalosis. This type of alkalosis, mostly with low chloride and low potassium, is called low chloride and low potassium alkalosis, a metabolic disorder specific to pyloric obstruction. Due to the lack of potassium in the blood, potassium ions in the distal renal tubular cells are also reduced, so only hydrogen ions (H+) are exchanged with sodium ions, and the amount of urinary excretion of H+ increases, making the urine acidic. Patients with this kind of metabolic alkalosis thus have the paradoxical phenomenon of acidic urine, which is also unique to pyloric obstruction, indicating the presence of low blood potassium in addition to hypochlorine alkalosis.
(2) Local pathophysiological changes.
Pyloric obstruction often develops gradually, i.e., from partial obstruction to complete obstruction. In the early stage of obstruction, in order to enable the discharge of chyme into the duodenum, gastric peristalsis is enhanced and the muscle layer of the gastric wall is compensatory hypertrophy, but the stomach is not significantly enlarged. With the increasing obstruction, although the stomach has strong peristalsis. It is difficult to overcome the resistance of the pylorus, the stomach is gradually dilated, peristalsis is weakened, the gastric wall is relaxed, gastric retention occurs, and the pouch is dilated.
Due to the retention of gastric contents, the mucosa of the pyloric sinus is stimulated to produce gastrin, which leads to increased secretion of gastric wall cells and inflammatory changes in the gastric mucosa, or even ulcers.