Inadequate Digestion Syndrome

This is a symptom complex characterized by digestive disorders in the gastrointestinal tract. Disorders can be associated with upset cavital diges­tion, i.e. in the stomach and the intestine (dyspepsia), and parietal digestion. Mixed forms also occur.

Aetiology and pathogenesis. Dyspepsia. This occurs due to non- compensated secretory insufficiency of the stomach, exocrine dysfunction of the pancreas, upset secretion of bile, disordered passage of chyme through the gastrointestinal tract (stasis, congestion due to stenosis and compression of the intestine, or accelerated passage due to intense peristal­ sis). Intestinal infection, dysbacteriosis, and alimentary disorders (overeat­ ing, diet rich in proteins, fats, or carbohydrates, intake of large amounts of fermented drinks) are also important. Dyspepsia may be functional, but commonly it is due to a digestive tract disease.'.«:« »,

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Chapter 7. Digestive System

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Pathogenesis: incomplete breakdown of food particles, active propaga­tion of bacterial flora in the intestine with its invasion of the proximal parts of the small intestine, dysbacteriosis, abnormally high activity of bacteria in the enzymatic decomposition of food with formation of toxins (ammo­nia, indole, low-molecular fatty acids, etc.) that irritate the intestinal muco-sa, intensify peristalsis, and cause symptoms of toxaemia due to their penetration into the blood.

Clinical picture. Gastric dyspepsia. This condition occurs in ach-lorhydria and achylia, long-standing decompensated pyloric stenosis, atrophic gastritis, and cancer of the stomach. The disease is characterized by the feeling of discomfort, pressure or distension in the epigastrium after meals, frequent eructation, regurgitation (often with acid or fetid odour), unpleasant taste in the mouth, nausea, and poor appetite. Achylous diar­rhoea and meteorism are not infrequent. Examination of the gastric juice reveals achlorhydria or achylia (both hydrochloric acid and pepsin are ab­sent from the gastric juice).

Intestinal dyspepsia occurs in the presence of exocrine dysfunction of the pancreas, chronic inflammatory diseases of the small intestine, and some other conditions. It presents as inflation and rumbling in the abdo­men (borborygmus), intensive passage of flatus, diarrhoea with putrefactive or acid smell and (in rare cases) constipation. Coprologic findings: steator-rhoea, amylorrhoea. X-ray findings: accelerated passage of the barium meal through the small intestine. Studies of the secretory function of the pancreas, aspiration biopsy, determination of enterokinase and alkaline phosphatase in the intestinal juice, and other tests help verify the cause of intestinal dyspepsia. Tests for hyperglycaemia with an oral starch load and radionuclide studies with glycerol trioleate, sunflower-seed or olive oil are used to estimate the degree of the cavital digestion derangement. The study of intestinal microflora is also important.

Treatment. This, in the first instance, is aimed at eradication of the un­derlying disease. Symptomatic therapy includes special diets and medica­tion for diarrhoea; enzyme preparations (pancreatin, abomin, festal), astringents, and carbolen are also administered.

Inadequate parietal digestion can be seen in congenital secretory insuffi­ciency of the intestinal wall (disaccharidase deficit enteropathy) and in chronic diseases of the small intestine attended with dystrophic, inflamma­tory, and sclerotic changes in its mucosa, upset structure of the villi and microvilli, and their decreasing number, deranged intestinal peristalsis (enteritis, sprue, intestinal lipodystrophy, exudative enteropathy, etc.).

The symptoms, course, and clinical picture are the same as in intestinal dyspepsia and in the malabsorption syndrome (see below).

The diagnosis is established on the basis of determination of enzymes

(amylase, lipase) during their desorption in homogeneous preparations of the small-intestine mucosa specimens taken by aspiration biopsy. The glycaemic curve drawn after oral intakes of disaccharides and monosaccha-rides helps differentiate the syndrome of inadequate parietal digestion (flat curve after the intake of maltose, saccharose, lactose; normal curve after the glucose and galactose intake) from lesions of the small intestine that are attended with malabsorption of the products of food decomposition in the small intestine. After an intake of polysaccharides (starch) this syn­drome may be differentiated from inadequate cavital digestion. Aspiration biopsy reveals atrophy of the intestinal mucosa (indirect sign).

Treatment is aimed at the main disease. For methods of management of malabsorption syndrome see below. Symptomatic therapy includes en­zyme preparations (abomin, festal) and astringents (tannalbin, albin). The drugs are given per os.

Malabsorption Syndrome

This symptom complex is due to upset absorption in the small intestine. The syndrome often develops in combination with the syndrome of inade­quate digestion. Primary and secondary malabsorption syndromes are dis­tinguished.

Malabsorption is probably explained by congenital disorders in the fine structure of the intestinal mucosa and genetically determined intestinal en-zymopathy. The onset of the secondary malabsorption syndrome is due to acquired structural changes in the intestinal mucosa evoked by acute and chronic enteritis, sprue, intestinal lipodystrophy, exudative enteropathy, le­sions of the small intestine in amyloidosis, systemic scleroderma, and other disease conditions attended with digestive disorders. The upset intestinal digestion and accelerated passage of chyme through the intestine are deci­sive in acute and subacute diseases. In chronic conditions the decisive fac­tors are dystrophy and atrophic fibrous changes in the mucosa of the small intestine, shortening and levelling of the villi and crypts, significant reduc­tion of the microvilli number, fibrous tissue formation in the intestinal wall with impairment of blood and lymph circulation, and disordered parietal digestion. All these changes limit absorption of the products of hydrolysis of proteins, fats, and carbohydrates, and of mineral salts and vitamins in the intestinal wall (see Alimentary dystrophy).

Clinical picture. Course. Gradual wasting, symptoms of metabolic dis­orders of all types (protein, fat, vitamin, water-salt), dystrophic changes in the internal organs with their subsequent dysfunction, and also constant steatorrhoea, creatorrhoea, and amylorrhoea are characteristic. Hypo-proteinaemia develops (mostly at the expense of reduction of the serum

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albumin level); hypocholesterolaemia, hypocalcaemia, and moderate hypoglycaemia occur. Hypoproteinaemic oedema develops in the presence of hypoproteinaemia below 40-50 g/1. The characteristic symptoms of poly-hypovitaminosis are osteoporosis, anaemia (hypochromic anaemia in predominant malabsorption of iron, and hyperchromic anaemia in upset absorption of vitamin B12), trophic changes in the skin, nails, progressive atrophy of the muscles, signs of polyglandular insufficiency, weakness, and (in severe cases) acidosis and cachexia.

Diagnosis. Laboratory examinations determine hypoproteinaemia, hypocholesterolaemia, hypoglycaemia, and other disorders due to malab­sorption.

Coprologic studies reveal increased content of undigested food in the faeces and also increased excretion of the products of enzymic decomposi­tion of food. Enterobiopsy reveals atrophic changes in the mucosa of the proximal parts of the small intestine. Since the walls of the small intestine absorb great amounts of various substances, different methods are used to study their absorption. These are tests with carotine, folic acid, galactose, D-xylose absorption test, etc. Caseine, albumin, oleic acid, methionine, gly-cine, vitamin Bi₂, folic acid, and other substances labelled with radioactive isotopes have recently beed used. The method is based on the determination of concentration of labelled substances and the time of their appearance in the blood, their excretion with the urine or faeces, and assessment of residual radioactivity of faecal masses that is indicative of the amount of unabsorbed substances. Determination of the absorbed nutrients is based on the study of the chemical composition of food and stools during a cer­tain period of time.

The course of the disease depends on the underlying condition and prospects for its cure. The prognosis is unfavourable in severe cases.

Treatment. The underlying disease should be treated. Symptomatic treatment: parenteral nutrition, administration of vitamins, plasma, protein hydrolyzates, glucose, nutrient enema, correction of electrolyte metabolism.

Prophylaxis includes timely treatment of diseases that usually concur with the malabsorption syndrome.