ence of gastric secretion or retention on the percentage of salines in the blood. The sodium chlorid is most reduced in this manner, and the plasma may thus become hematocytolytic. 6. Clinical observation teaches that chronic irritation of the abdominal sympathetic exerts a depressing influence on the regeneration of the blood, particularly as regards the development of the hemoglobin of the red corpuscles. The action of the irritable abdominal sympathetic (gastroptosis, adenohypersthenia gastrica, neurasthenia gastrica) is the most common cause of simple and of chlorotic oligochromemia. 7. Peptonization and peptone absorption are causes of physiological leukocytosis, and in the advanced stages of some of the diseases of the stomach this digestive leukocytosis is not excited. As a consequence the resisting power (healing and phagocytosis) of the system is diminished, and the normal quantity of albumins in the plasma is not maintained. Leukopenia may be produced by subnutrition or by the absorption of the unconverted products of albumin digestion. 8. Pathological leukocytosis may develop in carcinoma and in the diseases of the stomach with inflammatory complications. As regards the diseases of the red corpuscles, diseases of the stomach may produce either oligochromemia or oligocythemia. Oligochromemia is always dyshematopoietic, unless it represents the regeneration period of oligocythemia. The disease and the symptom may be readily distinguished by the clinical history and by the microscopic and staining properties of the blood. Oligocythemia, on the other hand, may be dyshematopoietic, hematocytolytic, or degenerative. The diseases of the stomach never cause the red corpuscles to undergo primary degeneration. Consequently, oligocythemia of gastric origin is always due either to insufficient and defective development of the blood or to the excessive destruction (or loss by hemorrhage) of the red corpuscles. These two forms of oligocythemia may be readily distinguished by the signs of dyshematopoiesis and by the signs of hematocytolysis, a discussion of which here would lead too far from the original subject. Of the diseases of the white corpuscles, leukemia is never produced by the diseases of the stomach. But digestive leukocytosis may not occur, pathological leukocytosis may be persistently present, the white corpuscles may degenerate (as many as ten per cent. of them may display the degenerative changes), or leukopenia may represent the chief alteration of the blood. The plasma may be altered qualitatively or quantitatively and become as a consequence hematocytolytic, or the total volume of the blood may be decreased. The changes of the blood which are produced by the diseases of the stomach are not so constant or so characteristic as to enable us to reason back from the disease of the blood, to the particular disease of the stomach which has caused it ; but a particular disease of the blood should direct the search for the group of diseases of the stomach which may cause it, and the blood changes have some diagnostic value in the differentiation of one disease or group of diseases of the stomach from another. The blood changes produced by the particular diseases of the stomach have been described under the symptomatology of those diseases. IV. INFLUENCE ON NUTRITION. Not every disease of the stomach disturbs nutrition. In some cases the digestion and utilization of the food may be normal; assimilation and disassimilation may go on as in health; enough food may be ingested and retained to supply the needs of nutrition. But such is not always the case, not even in the dynamic affections of the stomach nor in the mild. forms of its anatomical diseases. The acute diseases of the stomach may rapidly affect nutrition, and the chronic diseases seldom run their long course without producing subnutrition or without disturbing the processes of nutrition. The most frequent of these disorders of the processes of nutrition are excessive nitrogenous waste, uricemia, and phosphaturia. Subnutrition may be caused by a disease of the stomach in a number of ways, and it may vary in degree and in the rapidity of its development. The diet is often insufficient on account of loss of appetite, on account of disgust for some one of the grand classes of food, on account of a desire to avoid the pain or discomfort of digestion, or on account of an injurious plan of alimentation. Moreover, when the alimentation is sufficient, a portion of the food may be lost by vomiting, by fermentation, by putrefaction, by diarrhea, or by failure to digest and absorb it to the same degree as in health. In the advanced cases of anorexia nervosa the patient presents a picture of slow and self-inflicted starvation, and the loss of appetite in the anatomical diseases like carcinoma, chronic asthenic gastritis, and acute gastritis is one of the causes of subnutrition. The pain of ulcer, of chronic hypersthenic gastritis, of adenohypersthenia gastrica, or of carcinoma, the discomfort of neurasthenia gastrica, and of hyperesthesia gastrica, and of the diseases accompanied by retention and by stagnation, often force the patient to diminish the quantity and to contract the variety of the food below the requirements of the body. Moreover, chronic pain itself exerts a depressing influence on digestion and is a cause of emaciation. Frequently repeated alimentary vomiting, whether it be nervous, central, or reflex, or symptomatic of a disease of the stomach, may produce subnutrition as surely as does the failure to eat enough to support the body. In myasthenia gastrica and in pyloric obstruction-briefly, whenever motor insufficiency exists-nutrition is in more or less danger; if there be only stagnation, the influence on nutrition is determined by the degree of fermentation of the chyme; while if there be retention, the body may starve for lack of both food and water. It is well known that the intestines are capable of doing all the digestion and absorption that the body requires, but motor insufficiency may withhold the opportunity to establish digestive compensation. The disturbances of secretion may also produce subnutrition. If secretion be excessive,—as in adenohypersthenia gastrica, in chronic hypersthenic gastritis, and in ulcer, the digestion of the starches is interfered with in the stomach, and the excessive peptonization of the albumins may increase intestinal putrefaction and produce intestinal irritation and diarrhea. Nature here does what the physician often causes when he prescribes the digestive ferments and peptonized foods. If secretion be diminished, the albumins may not be properly digested, but the salivary digestion of the starches is more active than in health, and the intestines, if they be healthy, are likely to establish digestive compensation. But it often happens that loss of appetite, pain, faulty alimentation, vomiting, disorders of secretion, motor insufficiency, fermentation, and an abnormal chyme act more or less in concert, and produce subnutrition which is more or less rapid and grave. Excessive nitrogenous waste may be caused by a disease of the stomach. In subnutrition not only the body fat but also the body protoplasm is destroyed. The organism eats itself-lives on itself. But in carcinoma, in some cases of acute mycotic gastritis, and, probably, in some forms of gastric auto-intoxication, nitrogenous catabolism is in excess of the requirements of the body. The hyperazoturia manifests a purposeless waste of albumin. The inference seems plausible that the excessive destruction of cellular protoplasm is due to protoplasmic poisons formed in the neoplasm or in the contents of the stomach. The diseased stomach may cause accumulation of uric acid in the system by producing acid auto-intoxication. The socalled uric acid diathesis is not a morbid entity with one cause, but it is a chemical condition which is variable in its manifestations and complex in its causation. The accumulation or precipitation of uric acid in the organism is the result of pathological chemistry, and is the expression of a series of diseases which are commonly classified as gouty. There is no insufficient oxidation, for uric acid is the end product of nuclein waste. There may or may not be an excessive formation of uric acid. There may or may not be retention of uric acid as a result of the insufficiency of the eliminating organs. There may be no quantitative anomaly, but only a change in the form in which the uric acid exists, as a result of the altered reaction and composition of the fluids of the body. It is probable that uric acid circulates in the body as a quadriurate, or as a biurate in combination with the neutral phosphate of soda. Be this as it may, the precipitation of the uric acid is prevented by the accompaniment of a sufficient proportion of the neutral disodic phosphate. If the biurate or quadriurate increases proportionately beyond a certain limit, or if the neutral phosphate of soda decreases beyond a certain limit, there will be precipitation. Consequently, the precipitation of the urates is inaugurated either by a diminution of the available neutral phosphate or by an increase of the uric acid. Furthermore, the available neutral phosphate may be decreased by a diminished supply of protecting alkalies or by an increased supply of converting acids. We therefore recognize three grand forms of the uric acid diathesis or uric acid precipitation: I. Gastro-intestinal form. (a) Acid fermentation. (b) Excessive pancreatic and intestinal secretion. 2. Nutrition form (excessive formation of acids: phos- (a) Defective alimentation. (b) Excessive catabolism. 3. Retention form (defective elimination of acids). (a) Insufficiency of the skin. (b) Insufficiency of the kidneys. The gastro-intestinal form of the uric acid trouble is due to the excessive acidity of the system and to the resulting diminution of the quantity of the neutral phosphate of soda which is available for holding the uric acid compounds in solution. The stomach removes the chlorin to form hydrochloric acid, and leaves the alkaline base of the chlorid for the protection of the neutral phosphate. The excessive secretion of the intestines and of the accessory digestive glands removes too much of the protecting alkalies. Fermentation produces acid self-poisoning. The result is excessive acidity or diminished alkalinity of the fluids of the body. diminution of the available neutral phosphate of soda, and precipitation of the uric acid compounds. Ninety grains of bicarbonate of soda administered before breakfast is sufficient, in health, to neutralize the acidity of the system and to render the urine secreted during the following two hours neutral in reaction. If the urine, on making this test, does not become neutral, its acidity is the exact index of the excessive acidity of the system. The gastric form of gout results only from a chronic disease of the stomach, and is most frequent when the diminished gastric secretion and gastric fermentation are accompanied by excessive intestinal secretion. Chronic asthenic gastritis with motor insufficiency, carcinoma, and myasthenia with diminished secretion are the most common diseases of the stomach which may produce uric acid precipitation and retention. As with uric acid in the uric acid diathesis, so is it with phosphoric acid in phosphaturia: it is not the quantity, but the form, of the uric acid and of the phosphates which is important. The acidity of the urine is diminished until it is nearly neutral, or neutral or even alkaline, and the phosphates precipitate in it either spontaneously or on heating. The quantity of the acid phosphates is diminished and the quantity of the neutral and alkaline phosphates is in excess. Instead of increased there is diminished acidity of the fluids of the body, which is not incidental to alimentation, though it may be produced and controlled by it, but which is a chemical condition due to excessive elimination of acids, accompanied often by diminished removal of alkalies by the intestines. During the period of normal gastric digestion the acidity of the urine is diminished, and this condition of the urine results from the withdrawal of acid from the body by gastric secretion. The degree of change of the acidity of the urine during digestion, and under the same conditions, is a rough index of the amount of acid secreted by the stomach. |