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Gastroparesis - Delayed stomach emptying

Gastroparesis  (Delayed Stomach Emptying)

  What is gastroparesis?

  What causes gastroparesis?

  What are the symptoms of food sitting too long in stomach?

  Complications of gastroparesis

  How does gastroparesis typically occur?

  Who has gastroparesis?

  Physiology of gastroparesis

  How to treat gastroparesis?

 

What is gastroparesis?

 

      Gastroparesis is a disease or disorder of the muscles of the stomach or the nerves controlling these muscles that causes them to stop working - This results in the stomach taking too long to empty its contents into the intestine and an inadequate grinding of food.

 

What causes gastroparesis?

 

      Normally, contractions are modulated by the Vagus Nerve under central nervous system control – which modifies gastric and sphincter contractility in response to feedback from:

 

-       Stimulation after eating - causes gastric contractions to propagate through the stomach;

 

-       Various intestinal peptides -  E.g. motilin and cholecystokinin;

 

      Gastroparesis is usually a consequence of:

 

-       Any disruption in the timing or strength of normally propagated gastric contractions (i.e. unsynchronized muscle contraction and relaxation / too weak / not frequent enough contractions) – and  will cause food not to be propelled forward towards the small intestine for further digestion;

 

-       Non-opening of pyloric sphincter (valve at bottom of stomach) its contracting too strongly prevents release of food into small intestine.                    

 

What are the symptoms of food sitting too long in stomach?

 

      Nausea, vomiting, excess belching, reflux of stomach acid and bloating – are the common symptoms of dysmotility;

 

      Abdominal pain;

 

      Some people feel full and uncomfortable even after just a few mouthfuls of food;

 

      Some feel lethargic

 

Complications of gastroparesis

 

      Bacterial growth in the stomach – from fermentation of the stomach contents when it lingers too long.

 

      Food can harden into solid masses (called bezoars) that may cause nausea and vomiting. Bezoars can be dangerous if they obstruct the passage of food into the small intestine.

 

      Can make diabetes worse - when food delayed in the stomach finally enters the small intestine and is absorbed, blood glucose levels rise. Since gastroparesis makes stomach emptying unpredictable, blood glucose levels can be erratic and difficult to control.

 

 

How does gastroparesis typically occur?

 

      Triggered by certain foods, way of eating, infections, medications E.g.  Fatty and rich foods, too much alcohol, eating late at night, eating on the go, viral stomach upset or taking antibiotics.

 

As a complication of:

 

·    Diabetes (common cause, damages vagus nerve)

·    Parkinson’s disease

·    After stomach or vagus nerve surgery

·    Hyperthyroidism

·    Anorexia nervosa

·    Paralysis

·    Postviral syndromes

·    Smooth muscle disorders

E.g. amyloidosis, scleroderma

 

      Imbalance of magnesium, calcium, potassium – these minerals are important operators in muscle function; ideally calcium intake should be twice that of magnesium, but typically in a Western diet, intake is  ~4 to 1 and magnesium deficiency in the body is common

 

      Side-effect of medication – particularly those that slow intestinal contractions; E.g. narcotic pain relievers, opiates;

 

      Damaged vagus nerve  (vagal neuropathy) – the vagus nerve controls movement of food through the GI tract, but if damaged, it can send wrong or weak signals between the body and the brain.  The vagus nerve can be damaged by:

 

         Surgery on the esophagus or stomach

         Injury or upper respiratory infections

         When blood glucose remains high for an extended time - as in diabetes and thyroid disease.

         Alcoholism - found to contribute to vagal neuropathy.   

 

      Vagal nerve neuropathy can be reversed – if, when possible,  measures are taken to eliminate the cause of the condition. E.g. diabetics who control their blood sugar, alcoholics who decrease their alcohol intake, or those recovering from severe upper respiratory infection may regain normal vagal nerve function

 

Who has gastroparesis?

 

      More common in women - a hormonal link has also been suggested, as gastroparesis symptoms tend to worsen the week before menstruation, when PROGESTERONE  levels are highest. Dysmotility can also affect men and children;

 

      A study of 146 patients with gastroparesis - seen over 6 years at a referral center demonstrated that:

 

         35% had idiopathic gastroparesis;

         30% had diabetic gastroparesis;

         13% had gastroparesis related to surgical injury of the vagus nerve;

          7.5% of cases were related to Parkinson's disease or other neurologic conditions;

         4.5% were related to intestinal pseudo-obstruction;

         Remaining 10% of cases included other miscellaneous conditions - specifically connective tissue diseases, such as scleroderma.

Soykan I, Sivri B, Sarosiek I, et al. Demography, clinical characteristics, psychological abuse profiles, treatment, and long-term follow-up of patients with gastro paresis. Dig Dis Sci. 1998;43:2398-2404.

 

 

Physiology of gastroparesis

 

  

      Normal Food path from stomach to small intestine – the stomach is a muscular sac about the size of a small melon, that expands when you eat or drink to hold as much as a gallon of food or liquid. The stomach mechanically churns and pulverizes your food while hydrochloric acid (HCl) and enzymes requiring an acid environment break it down. Muscle fibers of the stomach wall create structural elasticity and contractibility, both of which are needed for digestion and propelling food towards the intestines.

 

      Pyloric Sphincter/Valve controls release of food from the stomach

 

-       The pyloric sphincter (valve between stomach and intestines) stays closed while food is being digested in the stomach  (to keep the food inside the stomach) - while strong muscular contractions (peristaltic waves) push the food toward the pyloric valve, which is the gateway to the upper portion of your small intestine (duodenum);

 

-       When HCl and the stomach enzymes have had enough time to do their job, alkaline bile (from gall bladder) and pancreatic juices (a watery bicarbonate solution) are secreted into the upper small intestine (duodenum) - to prevent damage to the duodenum when the stomach’s highly acidic contents are released;

 

-       Once the duodenum has become strongly alkaline, the pyloric sphincter receives a signal to open, and the partially digested food is released into the small intestines - where most of the absorption of nutrients takes place.

 

         Chronic dehydration will prevent pyloric valve from opening – due to an insufficient water supply in body’s circulation from which the pancreas can produce the watery bicarbonate solution required to protect intestinal lining from stomach’s acidic contents

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