Complete Text (Part 3)

intake. 3. Pressure and yelocity of blood current. 4. Condition of renal parenchyma. 5. Loss of fluid by other means: perspiration, res- piration, intestines, formation of transudates and exudates. _ 6. Vasomotor phenomena. The normal excretion yaries bet^yeen 900 and 1200 cc per day. • - Functional capacity is. from 20 -tjo- Bo- liters. Often on forced T^~ater 9 to 10 lifers are ex- creted in typhoid without damage to the kidney. Normally at night less is excreted than during the day, the ratio being 100 parts by day to 60 — 80 parts by night. In some forms of nephritis, hepatic 31 insufficiencT aud cardiac disease, this ratio is re- versed. Nycturia signifies tlie excretion of more urine at night than during the day. It occurs character- istically in chronic diffuse nephritis. Polyuria signifies the excretion of 3000 cc or more urine per day. Causes : 1. Increased fluid intake. 2. Diuretics. 3. Nervous disorders. (a) organic; (b) func tional. 4. Diabetes mellitus and insipidus. 5. Chronic nephritis. 6. Absorption of exudates. 7. Epicritical (end states of acute febrile dis- orders ) . S. Sometimes in ureteral stricture. Oliguria signifies the excretion of 800 cc or less in 24 hours. Causes : 1. Decreased fluid intake. 2. Loss by other means. (a) phj^siological (b) pathological 1. Formation of exudates aiid transu^ dates. 2. Acute febrile states. •3.- Acute nephritis. ^ ..'...' i. End state of chronic nephritis. 5. Chronic diarrhoea. 6. Vomiting. Anuria signifies no urine. Causes : 1. Obstruction to urinary passages. 2. Reflex (functional neuroses^ Dietl's crisis). 32 3. Renal, acute nephritis, or end stage of chronic nephritis. 4. Prerenal conditions. Poisons : bichloride, arsenic, anaesthetics. Occasionally after veronal medication (S. R. Miller). Pollakiuria signifies nnduly frequent passage of urine. Occurrence : 1. Polyuria of nephritis. 2. Prostratic disease. 3. Bladder disease. 4. Ureteral stricture. Specific gravity. Methods of determination: 1. Balance picnometer. 2. Urinometer which is calibrated at 15 deg. C. The reading should be taken at the junction of the lower meniscus and flu^.d. The Sj). gr. depends upon the amount of urine excreted and the amount of solids therein. Sodium chloride and urea are the chief sources of high Sp. gr. in normal urine. Nor- mal urine has a Sp. gr. between 1015 and 1020 for 1200 to 1500 cc per day. Clinical value of specific gravity: 1. Estimation of total solids of urine. Haeser's coefficient equals 2.33 times the last two figures of the reading and gives the weight of solids per 1000 cc. Normally the total solids average from 60 to 70 grams per day on the basis of 1500 cc output. 2. Estimation of urea (Webster). 3. In polyurias, with low specific gravity, it points to chronic diffuse nephritis, and with high specific gravity to diabetes mellitus. 4. Oliguria, with low specific gravity, gives bad prognosis in nephritis. 33 5. Extensive oedema, with low Sp. gr., points to renal trouble. 6. Normally urines collected at intervals during the day show a variation in the Sp. gr. of 10 points. In chronic nephritis there is a tendency to the fixa- tion of the reading at about 1010 (Hyposthenuria). Reaction of the urine. Normal urine is faintly acid, partly from the acid sodium phosphate and partly from free acids, such as sulphuric, oxalic and hippuric, which occur when more animal than vegetable diet is taken. More acid occurs in the morning, and less after heavy meals. Variations in the total acids: 1. Use of drugs, sodium bicarbonate and acid sodium phosphate. 2. Hyperacidity increases; hypoacidity decreases acid. 8. Less after intestinal hemorrhage and after oedema due to nephritis. Classification of reactions : 1. Acid. 2. Neutral. 3. Amphoteric, effecting both red and blue litmus. 4. Alkaline. Alkalinity : 1. Fixed. 2. Volatile. Hold wet litmus in the fumes of the urine and the ammonia tliere present turns litmus blue. This condition leads one to suspect inflam- mation of the bladder. Acidity of urine is due to acid sodium phosphate (NaHoPO,^)* and free organic acids. 34 Quantitative determination of acids : Folin's method : Urine 25 cc. Powdered Potassium oxalate 5 to 20 grams (Prevents dissolution of salts of calcium.) 1% solution plienolphthalein 2 drops Titrate to the end point (a faint pink) with N/10 NaOH. The acidity is expressed in terms of : 1. Total no. of cc. necessary to neutralize total 24-hour output, 617 is about normal. 2. Percentage, number of cc. necessary to neutral ize 100 cc. of urine, 35 to -10 per cent normal. COLORING MATTER OF URINE The normal color of urine is a shade of yellow or amber. Ordinarily the color varies directly with the specific gravity, but here are tAvo exceptions : (1) Diabetes, which is associated with a faint yel- lowish green color and may have a Sp. gr. of 1040 or over. (2) Chlorosis, which may also be asso- ciated with a pale urine and high Sp. gr. Normal pigments of urine. I. Urochrome, which is responsible for most of the yellow color and Avhich is of little importance clinically. Also urocliromogen, precurser of uro- chrome. II. Uroerythrin, which is responsible for the sal- mon-red color. It is a pigment increased on exces- sive meat diet and in fevers. When extracted witji 35 amyl alcohol it gives characteristic spectroscopic bands. III. Urobilin, which is a complicated group of pigments, possessing a pyrrol nucleus. Xormal urine contains 30 to 100 mg. per 24 hours. IV. Urobilinogen, which is unstable and by sun- light is changed into urobilin. Origin of uroljilin : 1. Hematogenous theory, that urobilin may be formed directh' from the blood without the inter- vention of the liver. 2. Hepatic origin. Liver entirely responsible. 3. Nephrogenous theory, that under certain con- ditions the epithelium of the kidney changes bili- rubin into urobilin. 4. Enterogeneous theory, indicated by the dia- gram. Hcmogloltin I Biliruhin (action of the liver) I LrohiIi)i and uroljiUnogeii (action of intestines and bacteria) I I Portal system Part excreted in the feces I Liver I I 'Normal Abnormal I I Bilirubin (Failure to convert) Hemoglobin Urobilin absorbed and excreted by the kidneys. Significance of uro'biVmuria : 1. Bile is entering the intestines. 2. Extensive blood destruction. 3. Hepatic insufficiency. (a) Physiological. (b) Actual hepatic disease. 4. A certain amount of renal efficiency. 5. Absence of urobilin means total obstruction of the bile duct. 36 Occurrence of urobilinuria : 1. Common in hepatic cirrhosis. 2. Chronic passive congestion (prognostic evi- dence). 3. Hemolytic anaemia. 4. Malaria. 5. Pneumonia. Appearing at the time of the crisis is a favorable sign, especiall}^ if the patient is jaundiced before. If in the serum of such a patient the prognosis is usually hopeless. G. Measles and, scarlet fever and all affections which lead to liver damage. Appearance of tlie urine in uroNlinuria. The urine takes on a dark 3^ellowish color. Output is irregular and single void- ings sliOAV great variations in the amount excreted. Tests for urobilin: Schlesslnger's. To about 5 cc. of urine add a few drops of Lugal's solution, 1 to 2 cc. of NH^OH, and an equal volume of 10% alcoholic solution of zinc acetate. Filter and examine filtrate for greenish fluorescence. Spectroscopic examination : Extract with amyl alcohol. Alkaline solution gives broad band between E and F. Acid solution gives intensified bands in same place and the E — b space is filled. Ehrlich's 'benzaldekyde test. Use a 2% solution in concentrated HCl. Use 3 drops of this reagent to 3 to 5 cc. of urine. The pres- ence of a pyrrol derivative gives a cherry-red color. Heating before adding reagent gives intensification of same. 37 V. Iiulican (Iiidoxyl sulphate) 5 to 45 mg. per da 3^ Animal proteins alone give it. _, , ] indol ^ indoxyl Tryptophane= | ^^^^^^ absorbed= j ^^atoxyl These are conjugated with sulphuric acid and ex- creted as sodium or potassium salts. Indicanuria is increased upon a meat diet and is not excreted on a non-protein diet. Urine is generally normal color when voided, but on standing becomes dark. Formation : 1. Extra-intestinal, due to xDrotein decomposition in the body (bronchitis, abscesses and empyemias), 2. People with inborn errors of metabolism. 3. Gastro-intestinal tract diseases or disorders : (a) Transient phenomena, (b) Constant oc- currence, (c) Recurrent type due: 1, to pathological conditions of intestinal tract. 2. Perversion of intestinal tract secretion. Indicanuria is not necessarily associated with constipation, but is due to pathological conditions in the lining of the intestinal tract or of its secre- tions. Subacidity may give it. Tests for indican (Obermayer's). Equal parts of urine and reagent (0.2% solution of ferric chloride in fuming HCl). It is best to filter out bile pigments with PbSO^ before adding reagent. To the urine and reagent add 2 cc of chloroform and shake 12 times. Chloroform ex- tracts indican (blue), which sinks to the bottom of the test tube. KI gives a deep cherry red color with the same test. Albumin^ unless present in large amounts, does not interfere with the reaction. Thymol gives violet red shade, which is obviated with sodium thiosulphate. 38 VT. Hematoporphyriii. Occurs in uriue in such small amounts that it is normally difficult to detect. It is an iron-free derivative of hemoglobin. Increased amounts occur in: 1. Certain diseases, rheumatism, phthisis, Addi- son's disease, paroxysmal hemoglobinuria, exoph- thalmic goiter, lead poisoning, syphilis and other diseases. 2. Use of hypnotics such as trional, veronal, sul- pronal and tetronal. Test for HematoporiDhyrin. Strictly spectoscopic. Take 5 cc of urine and add 10 cc of 10% XaOH. Filter and to the precipitate add 5 to 10 drops of dilute HCl and 15 cc of alcohoL Filter and examine the filtrate spectoscopically. Abnormal pigments of the urine. A. Blood pigments : Hemoglobin, methemoglobin, hematin and hematoporphyrin. Occurrence : I. Hematuria. A condition in which blood as such is present in the urine, and is visible with the naked eye or with the microscope. The urine is turbid, red-tinged, smoky, and sometimes clots are seen. Occurrence of hematuria : 1. General diseases. Yellow fever, typhoid fever, smallpox, leukemia, and purpura. 2. Renal origin: (a) Acute congestion or inflam- mation, (b) acute congestion following poisons, (c) renal infarction, (d) stone in kidney, (e) tbc. of kidney, (f) tumors of kidney, (g) parasites, such as filaria and bilharzia. 8. Genitourinary tract conditions : Passage of stone, Dietl's crisis, stone in bladder, tumors of bladder, and urethral conditions similar. 4. Traumatism, o^Derative or accidental. 5. Renal epistaxis. In this condition sudden 39 unexplained liemorrliages occur with no pain. It occurs in one or the other kidney and does not lead to more serious conditions later on. IT. Hemoglobinuria. In this condition the formed elements of tlie blood are absent and merely the pig- ments are present. The urine is usually clear and dark brown. Occurrence : 1. Toxic conditions, following severe burns, expo- sure to cold, poisons and fevers. 2. Essential or paroxysmal type characterized clinically by: (a) Pronounced hemoglobinuria. (b) Aching in the lumbar region. (c) Chills, fever and headache. This type often follows exposure to cold. In this condition the patient's own blood has amboceptor, Avhich is capable of uniting with patient's own cor- puscles. Cause not known. Majority are spyhilitics, acquired or congenitally so. Tests for hlood and hemoglobinuria: Chemical tests. 1. Heat and acetic acid test. Brown coagulum forms, which tends to float. Decolorized with acid alcohol. 2. Heller's test. Make urine alkaline with sodium or ammonium hydroxide, gently warm. A precipi- tate of phosphates and carbonates forms, which turns brown. 3. Teichmann's hemin test. To urine add XaOH. Filter and wash with water. Dry by pressing be- tween filter papers. Fragments of ppt. are placed upon glass slide, to which is added a crystal of XaCl. Add three drops of glacial acetic acid and place cover slip over mixture. Heat gently, do not 40 boil, and as acid evaporates replace it. As soon as the material becomes brown, allow to cool slowly. A positive test shows, microscopically, crystals rhomboid in shape and in sheathes. These crystals are hyprochlorate of hematin. Errors : 1 . Heating too much. 2. Too rapid cooling. 3. Excess of NaCl. Sensitive in dilution 1 to 100,000 parts. Giiiac Test: For blood — 1. Make fresh tincture of guiac with alcohol; should be shade of light yellow ; mix with equal vol- ume of ozonized oil of turpentine, or HoOg. 2. Four or five cc urine, to 0 to 8 drops glacial acetic acid ; allow to stand 8 minutes ; extract with ether. Pour solution 2 upon 1 in such manner as to form layer ; a deep blue ring will form if blood is present. Benzidine Test for Blood — 1. Two per cent, alcoholic solution is taken and mixed with equal volume ozonized oil of turpentine, or H2O2. 2. Four to five cc urine plus 6 to 8 drops glacial acetic acid; let stand 8 minutes and extract with ether. Stratify 2 upon 1; a greenish ring will form at line of contact if blood is present. III. McthemogJoljin. Occurs in spontaneous de- composition of blood ; also following poisoning by the chlorates, nitrates, arsenic, acetanilid, antipyrene. sulphonal, turpentine. IV. Hematoporpliyrin. See previous discussion. B. Bile pigments. Bilirubin is the most frequent. Sources of choluria (a) Hepatic origin. (b) Hematogenous origin. 41 K- ^- o I ^ ^ ^ ^ I \i- 42 Hepatic origin occurs: 1. Cirrhosis of the liver, 2. Cancer of the liver. 3. Obstruction to the biliary passages. Hematogenous origin occurs : 1. AVhere blood pigments are present in ex- cess of the mobilizing power of the liver, as in pernicious anaemia, ma- laria, pneumonia, yellow fever. (All jaundice is essentially obstructive in origin.) Appearance of the urine in choluria : greenish yellow, brown, pure green. * Tests for l)ilc' : 1. Foam test. Shake a specimen of urine which produces foam. If bile is present the foam x:)ersists and is of yellowish color, ^'ormal urine does not produce much foam, and the foam which is produced is white in color. '2. (xmelin's test. Kegent : Strong HNO3 pl^^s HNO,. This can be made by boiling con. HNO3, in which is placed a match stick, until it takes on a yellowish color. Method : The urine is layered upon the reagent thus made. A positive test shows a green ring at the line of contact, and a yellow ring slightly above. Below the line of contact appear a series of colors ranging from blue to red from above downward. Errors: 1. Too much NHO,. 2. Too much albumin. :]. Urine containing too much indican. 4. Urine too concentrated. 5. Urine containing antipyrene or thymol. These drugs can be ruled out satisfactorily. 43 Rosenhacli's modification of GmelUi's test. Acidif}' urine Avith HCl and filter 4 or 5 times through same filter paper. Let paper dry. Touch a single drop of HNO, plus HNO, solution to the paper. Concentric rings will appear, green on the outside. Smithes test. Make urine acid with 5% acetic acid. Layer upon urine 1% alcoholic solution of iodin. Bile pigments give emerald green at line of contact some time after, which tends to diffuse upward. (Kather indefinite test.) Nakayama^s test. To 5 cc. of urine add from 5 to 10 cc. of 10% solution of barium chloride. Kemove ppt. by decantation. Treat the ppt. with the follow- ing reagent : 95% alcohol 99 cc. Con. HCl 1 cc. Ferric chloride .4 gm. Bring slowly to a boil. Bile pigments give emerald green. If urine changes to green, add HNOg and get red color. (Indefinite test.) C. Melanin. Normal j)ignient of hair and choroid coat of the eye. Pathological increase due to over-activity of the cells which form it. Occurrence: Melanotic sarcoma, Addison's dis- ease, ochronosis and sometimes in malaria. Urine is colorless when excreted, but turns dark either upon standing or the addition of alkaline or oxidizing agent. 44 Tests: All three of the following must be posi- tive : 1. Ferric chloride gives black ppt. 2. Precipitate soluble in sodium carbon- ate (black). 3. Mineral acids plus sodium carbonate solution give black ppt. D. Alkapton hoclies. When in urine designated alkaptonuria. Occurs in people who have an inborn hereditary error in metabolism. It is characterized by the inability of the body to break up the benzene ring. Tyrosin and phenylalanin are changed to uroleucin and homogenstic acid. Urine is nor- mal in color when voided, but becomes dark on standing. Occurs in children Avhose parents are lir.>t cousin?. It is a life-long condition, but not dangerous. Sometimes victims develop ochronosis. E. FJieuoJ do ivatii'cs. These substances consist of sulphuric acid in conjugation with phenol para cresol, pyrocatechin, and hydroquinone. They are excreted mostly in conditions associated with ijutre- faction in the intestinal tract or elscAvhere in the body. Sources: (a) Administration of drugs, (b) Pro- tein metabolism. F. Diazo compounds, due to alloxyproteic acid. Tests : Ehrlicli's Diazo Reaction. Reagent : Solution a. Aqueous sol. sodium nitrite 0.5 % Solution b. Sulphanilic acid 5 grams Concentrated HCl 50 cc. Water q. s. ad 1000 grams 1 part of sol. (a) plus 50 parts of sol. (b) plus equal vol. of urine. Shake quickly. Add .1 volume of 45 NH^OH aud shake quickly. A positive test is a deep- red color throughout the urine and a red foam. Red foam is the most important. After 12 hours a gran- ular greenish precipitate occurs. When doubtful, wait for this test. Xaphthalene, opium, chrysarobin and otlier drugs may give color quite similar, but the foam is not red and no greenish ppt. is obtained. Occurrence: The diazo reaction is never found in health. It does occur in typhoid fever, where it finds its most useful application. It is said to occur in the first or second week of the divsease in 80% of the cases. In case of relapse the test again becomes positive. The reaction also occurs in pneu- monia,