Page created on February 3, 2019. Last updated on May 25, 2019 at 21:57
Vomiting causes loss of stomach acid, causing (chloride-responsive) metabolic alkalosis. Severe vomiting can cause ruptures of the oesophagus, a condition called Mallory-Weiss syndrome.
Vomiting is the most frequent disorder of gastric emptying. It’s a defence mechanism used to get rid of potentially dangerous substances. It’s commonly preceded by nausea. Parasympathetic tone always increases during vomiting.
Vomiting involves closing the pylorus, retroperistaltic movements in the intestines, high abdominal pressure, and opening of the cardia and lower oesophageal sphincter. The increased abdominal pressure comes from the contracting abdominal muscles and diaphragm. Gastric content is forcibly emptied through the open cardia with projectile character, called projectile vomiting.
The increased abdominal pressure compresses the inferior vena cava, which decreases preload and causes a compensatory tachycardia. Later will the parasympathetic tone cause bradycardia.
The following factors can evoke vomiting:
- Hepatic congestion
- Mesenteric disorders
- Diseases that cause severe pain
- Acute myocardial infarct
- Kidney stone, gall stone
- Hypersensitivity of the “vomiting centre” in the brain or area postrema
- Bleeding into the stomach
- High intracranial pressure
- Toxic substances and drugs
- Heavy metals
- Uraemic toxins
- Fear, anxiety
- Sensory (taste, smell, sight, pain)
- Motion sickness
Vomiting isn’t a big deal if it occurs once or twice now and then – it mostly just causes mild salt, water and acid loss. However, we may have some severe consequences. In the case of a series of strong and severe vomiting can the strong forces lacerate the oesophageal mucosa, which causes haematemesis. This condition is called Mallory-Weiss syndrome. Vomiting may lead to aspiration, especially in patients with disordered consciousness.
Repeated vomiting leads to so much loss of acid that metabolic alkalosis occurs. So much fluid is lost that exsiccosis occurs with hypovolaemia. This causes secondary hyperaldosteronism, which stimulates Na+/K+ and Na+/H+ exchange in the distal tubules. This causes the tubular cells to be filled with K+ and H+ as they reabsorb Na+ from the filtrate and transport it back into the plasma. The tubular cells can’t deal with the extra K+ and H+, so it excretes it into the filtrate, which gives kaliuria and aciduria despite the alkalosis. This causes hypokalaemia and worsens the alkalosis.
Nausea itself stimulates ADH release and so does hypovolaemia. This may result in hypotonicity, which may induce further vomiting, perhaps due to increased intracranial pressure.
Acetonemic vomiting, nowadays called cyclic vomiting syndrome, is a special case of chronic vomiting that occurs mostly in infants. One theory is that a deficiency of gluconeogenetic enzymes is involved. This causes the infants to enter ketosis between meals, as the liver can’t sustain a normal blood glucose level in these periods. The ketonaemia causes vomiting.
A more modern theory involves a connection with migraines.
2. Disorders of gastric filling and emptying
4. Pathophysiology of GIT-peptides