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 PERITONITIS IN BIRDS.

From caponizing, accidental traumas, ruptured oviduct, perforations of bowels

by foreign bodies or worms, pyogenic susceptibility slight. Symptoms: inappetence,
drooping head, wings, tail, erect plumage, stiffness, straining, tense, tender,
pendent belly. Treatment: unload cloaca, puncture and irrigate abdomen,
laxatives. Prophylaxis, by laxative food, expulsion of worms, antisepsis in
operations, unloading cloaca, etc.

Causes. Male birds contract peritonitis from caponizing, and other

penetrating wounds of the abdomen, from rupture of the oviduct
impacted with egg matter, from perforations of the intestines by
foreign bodies, and from perforations by worms.
The danger from ordinary pyogenic germs is, however, at its
minimum, since birds stand at the opposite extreme from the horse,
and their wounds rarely suppurate.
Symptoms. The bird loses appetite, droops head, wings and tail,
ruffles its feathers, walks stiffly and heavily, and expels fæces with
much effort and even with cries. When caught the abdomen is found
to be full, tense and pendent and very tender to the touch. There is
more or less hyperthermia (108° and upward), and the subject
becomes more and more dull, stupid and feeble until death.
Treatment. In certain cases relief may be had by the unloading of
the cloaca, or the evacuation of peritoneal fluid, followed by
antiseptic, irrigation of the cavity. Laxatives may also be resorted to.
The most important measures are however prophylactic, and run in
the direction of careful manipulation and antisepsis in caponizing,
the unloading of impacted cloaca, before it has developed serious
disease, the maintenance of a suitably laxative diet, and the
prevention and treatment of worms. In case of tumors causing
chronic peritonitis, laparotomy can be resorted to with great
confidence.
 ASCITES IN SOLIPEDS.

Causes: follows peritonitis, obstruction of portal vein, tumors, hepatic diseases,

pressure on posterior cava, dilated right heart, heaves, ovarian disease, nephritis or
kidney degeneration, hydroæmia. Symptoms: slow advance, pot-bellied, with
fluctuation, hollow above, dropsy in limbs, sheath and under belly, percussion
sound flat below, weakness, debility, no fever. Diagnosis: Absence of fever, and of
fibrine, cells and granules in effusion. Lesions: those of primary disease, amount
and composition of effusion. Treatment: treat primary disease glandular swelling
or actinomycosis, iodide of potassium, remove diseased ovary or tumor, draw off
fluid, compress abdomen, saline laxatives, diuretics, iodides, pilocarpin, electricity,
bitters.

Causes. Ascites may be a remnant of a pre-existing chronic

peritonitis, or it may occur from any obstruction of the portal vein,
such as compression by organized false membranes, thrombus, in
the vessel, or pressure by lympadenoma in the portal fissure,
melanosis, sarcoma and other tumors. It results from cirrhosis and
other diseases of the liver which retard its circulation, from pressure
on the posterior vena cava, from insufficiency of the right auriculo-
ventricular valves, from dilatation of the right heart, and from heaves
or other obstruction in the pulmonic circulation. Other causes are
cystic or other disease of the ovary, diseases of the kidney and
hydroæmia, the latter two tending to general œdema as well as
ascites.
Symptoms. The disease comes on slowly and insidiously and at
first it usually passes unnoticed. When more fully developed the
abdomen is distended but somewhat pendent (pot-bellied),
fluctuating below, with falling in beneath the lumbar transverse
processes. Later the whole abdomen may be full, rounded, smooth
and tense, and the hind limbs œdematous to above the fetlocks or
hocks. There may be œdema of the sheath or lower wall of the
abdomen. Fluctuation can still be felt as a shock when an assistant
makes sudden concussion with the fist on the opposite side from that
on which the hand is pressed. This may be felt even more distinctly
by the hand introduced into the rectum. Percussion gives a flat sound
below and more or less resonant above. The pulse is small, weak, and
accelerated, heart beats irritable (sometimes palpitating), and
respiration labored and with lifting of the flank. From first to last
there is no hyperthermia.
If the cause is irremediable the issue is necessarily fatal sooner or
later.
Diagnosis from peritonitis depends largely on the absence of
hyperthermia, and of abdominal tenderness, and on the nature of the
ascitic fluid which is incoagulable, and comparatively destitute of
leucocytes cells and granules.
Lesions. The quantity of effused liquid is often enormous (50 qts.
Reynal, 80 qts. Woodger, 150 qts. Friedberger and Fröhner). It is
very watery and poor in salts and albuminoids, of a density near
1012, neutral or slightly alkaline, does not coagulate spontaneously,
and is not associated with false membranes. The peritoneum shows
no congestion, but is pale, and, like the abdominal walls, infiltrated.
Tumors, cysts and venous obstructions referred to under causes may
be found.
Treatment. When ascites depends on actinomycosis or glandular
enlargement a course of iodide of potassium may remove the cause.
In other cases an operation may remove the offending tumor or
ovary. Too often, however, the cause is beyond remedy and palliative
treatment only is available. The most urgent indication is the
removal of the accumulated fluid, and paracentesis under proper
antiseptic precautions is the readiest means to this end. Compression
by a tight bandage is necessary to prevent the sensation of vacuity
and tendency to fainting which come from the removal of the fluid
and to counteract the disposition to the instant effusion of more.
Even with the compress it is judicious not to draw off all of the fluid
at once in bad cases, but to make two or three operations and allow
the patient to become accustomed to the change in the intervals.
These may be repeated as circumstances demand. Saline purgatives,
or diuretics (saltpetre 1 oz., digitalis 25 grs., squill 3 ozs., iodide of
potassium 2 drs.), are useful, and pilocarpin is the most efficient
agent of this kind, but also dangerous by reason of the extreme
depletion which it causes. Electricity has been employed with alleged
advantage, also poultices of digitalis applied over the loins.
Cholagogues are also recommended especially in cases of liver
disease. Bitters may prove useful.
 ASCITES IN RUMINANTS.

Causes: as in horse, tuberculosis, in sheep distomatosis, chills when heated and

fatigued. Symptoms: pot-belly, fluctuating on percussion, gives flat sound, debility,
pallid mucosæ, sunken eyes, superficial dropsies on belly, in limbs, and under jaw,
in distomatosis, great emaciation, weakness, paperskin, ova of distoma in fæces.
Diagnosis: from ruptured bladder by passage of urine, and perhaps by sex, and
absence of urinous odor in liquid, from hydrometra by fluctuation over whole
belly. Lesions: those of solipeds, also tubercles or enlarged gall ducts with
distomata. Treatment: as for solipeds. Tuberculosis demands separation or
destruction, distomatosis, prevention.

Causes. These are in the main those which operate in the horse
and need not be repeated. In cattle, however, the affection is to a
large extent the result of abdominal tuberculosis, while in sheep it is
a constant result of advanced distomatosis. Gellé says it is common
in working oxen, which are turned out, hot and perspiring, to pass
the night in cold and wet.
Symptoms. The belly is enlarged and pendent, bulging out back of
the ribs, with fluctuation and dullness on percussion. The animal is
in very low condition, the mucosæ pale or yellowish white, the eyes
dull and sunken, panting and palpitations may be roused on the least
exertion, and swellings often appear along the lower aspect of the
body and between the branches of the lower jaw. In distomatosis it is
common to find dropsy of the chest, pallor and attenuation of the
skin, complete absence of the subcutaneous fat (paperskin), and
great emaciation and weakness. Ova of the distoma can be found in
the fæces. (See distomatosis). By turning the sheep on its back or
setting it up on its croup the percussion dullness will be made to
shift, always to the dependent part of the abdomen.
Diagnosis. From rupture of the bladder it is distinguished, by its
occurrence in females as well as males, by the absence of fever, and
of the complete suppression of urine and emptiness and tenderness
of the bladder which characterize the latter. Liquid drawn from the
abdomen has no urinous odor. From hydrometra, pyometra, and
hydramnios it is distinguished by the fact that the water accumulates
in the lower part of the abdomen, and is not confined to the womb.
On rectal exploration the outline of the empty womb is made out.
Lesions. Besides the lesions described for solipeds, one finds in
cattle, tuberculosis of the liver, spleen, and lymph glands, and
extensive clusters of tubercles on the peritoneum. In sheep the white
branching lines on the back of the liver may indicate the distension
of gall ducts infested by distomata.
Treatment does not differ from that recommended for solipeds. In
tuberculous cases, sanitary considerations demand the destruction of
the animal and disinfection of the carcass. In distomatosis treatment
must be preventive, as the distomata are difficult to reach with
vermifuges.
 ASCITES IN CARNIVORA.
Causes: obstructed flow of blood in hepatic, portal or renal veins, or in vena
cava, renal, heart, liver or splenic diseases, pulmonary congestion, asthma,
tuberculosis. Symptoms: pot-belly, hollow above, drooping back and loins, flat
percussion sound and fluctuation, change of position changes area of flatness,
anæmia, debility, scanty urine, diarrhœa, no fever. Diagnosis: absence of fever,
general fluctuation changing its seat by turning the patient, not confined to a given
organ like the bladder or womb. Lesions: quantity and composition of liquid,
lesions of primary diseases. Treatment: Correct if possible the primary disease,
evacuate the liquid, compress on abdomen, iodine solution for irrigation, saline
purgatives, diuretics, pilocarpine, bitters, iron, sunshine.
Causes. Ascites is generally the result of some obstruction to the
return of blood from some abdominal organ, but may also come from
renal disease, or hydroæmia in which general dropsy is likely to
occur. The dog is specially subject to heart disease, and disease of the
right heart (tricuspid insufficiency, dilatation, hydro-pericarditis,
fatty degeneration, etc.) throws the blood back on the whole venous
system and the extensive and dilatable portal veins are especially
liable to suffer. Diseases of the liver, so common in pampered house
dogs, still more directly block the portal circulation and induce
ascites. Tumors in the liver or spleen or in the lymph glands of the
porta act in this way, also cirrhosis, tuberculosis, cancer, hepatic
congestion, and degeneration. Constrictions of the vena portæ by
false membranes the result of former peritonitis must also be
recognized. As more distant causes, must be named obstruction to
the pulmonary circulation, as in congestion, asthma, tuberculosis
and diseases of the left heart. Seventy-eight cases were traced as
follows: to diseases of the heart and pericardium, 10; to tuberculosis,
8; to pleurisy, 4; to malignant tumors of the liver and lung, 2; to
hepatic disease without heart lesion, 3; to cancer of the liver, 1;
(Cadiot).
Symptoms. Enlargement of the belly is marked and peculiar, the
liquid accumulating below, pushing outward the lower ends of the
ribs, and making the lower part of the abdomen baggy while the
upper part, under the lumbar transverse processes, is flattened or
hollow. The back and loins droop forming a concavity superiorly, so
that the belly may almost drag on the ground. On palpation this
pendent abdominal sac gives the sensation of a mobile fluid without
the usual firm outlines of the intestinal masses, and when percussed
it gives out a flat, dull sound and produces a fluctuation or shock at
the opposite side of the abdomen. In the upper part of the abdomen
over the hollow flank more or less resonance is found. If the animal
is made to stand on his hind limbs the saccular dilatation and
flatness on percussion are in the region adjoining the pelvis; if held
up by its hind limbs they are transferred to the epigastric and
hypochondriac regions and the respiration is seriously interfered
with; if turned upon his back, the resonance is obtained on the linea
alba and at each side, while the percussion dullness is next to the
vertebræ. The clearness of the fluctuation is in ratio with the amount
of liquid present.
As in other animals, there are anæmia, pale mucosæ, poor
condition, thin, dry, unhealthy skin, weak pulse, irritable heart and
interference with respiration proportionate to the amount of liquid.
The urine is scanty, and there may be diarrhœa.
Diagnosis. From advanced or chronic peritonitis it is distinguished
by the history or evidence of diseased liver, heart, or kidney, the
absence of hyperthermia or abdominal tenderness, and the absence
in the ascitic fluid, extracted with a hypodermic needle, of blood
globules, or leucocytes in numbers, of false membranes, of excess of
salts, or of a tendency to coagulate firmly.
From overdistended bladder it is diagnosed by its slow, and
gradual development, and the change of fluctuation to the most
dependent part no matter what position is given to the patient,
whereas the tense bladder can be felt through the abdominal walls,
extending forward from the pelvis under all circumstances.
From ruptured bladder there is the same distinguishing feature of
slow development, the absence of symptoms of uræmic poisoning, of
tenderness of the bladder, and of suppression of urine, and also of
the urinous odor in the ascitic liquid obtained with the hypodermic
needle.
From advanced gestation the differentiation is found in the general
diffusion of the swelling and fluctuation, which is not confined as in
gestation to the mobile uterine horns, with a series of enlargements
each containing a solid nodular fœtus.
 From hydrometra and pyometra there are the same
pathognomonic differential features of the general diffusion of the
swelling among the intestines, and its accumulation in one
fluctuating mass at the most dependent part of the abdomen.
Tympany of the bowels causes uniform drumlike resonance, and
the swelling does not sag and fluctuate in the lower part of the
abdomen.
Abdominal obesity in old dogs gives the rounded swollen
abdomen, but there is an entire absence of the pendulous and
fluctuating features, and when punctured with the hypodermic
needle it furnishes no fluid.
From tuberculosis it is distinguished by the absence of nasal
discharge, or of tubercle bacilli in such discharge, or in the ascitic
fluid, and the latter inoculated on guinea pigs or rabbits does not
cause tuberculosis. The tuberculin test may also be resorted to.
Lesions. The liquid exudate has been found to amount to 30 or 40
quarts in large dogs (Hordt). It is often clear and translucent, of
amber tint, though in some cases it is slightly opaque, or reddish
yellow. It may remain fluid after extraction or again it may form a
loose jelly. It may be red in case of soft tumors or other neoplasms.
The liquid is very watery but may contain a considerable amount of
fatty globules or granules, and a few epithelial cells and leucocytes.
The peritoneum is pale or in advanced cases dull white from fatty
degeneration of the epithelium.
Treatment. The first consideration is the removal of the cause. If
this is a mere vicious action of the peritoneum, or the presence of a
thrombus, or of operable tumor, or even of curable disease of the
liver or kidneys, success may be hoped for, while in dilatation of the
heart, insufficiency of the cardiac valves, irremediable disease of the
lungs, liver or kidney, or malignant or inoperable tumor no such
result can be hoped for.
Apart from the removal of the cause the first indication is to
evacuate the liquid and this may be done with a large hypodermic
needle or small cannula and trochar inserted by preference on or
near the linea alba while the animal is in a standing position. Skin
and instrument should be rendered thoroughly aseptic, and a
bandage should be wrapped round the abdomen and gradually
tightened as the liquid escapes. This to a large extent obviates the
tendency to faint, or to cerebral anæmia which has caused sudden
death in a number of cases. It also to some extent counteracts the
sudden effusion of blood in the abdomen, which is at times
determined by the sense of vacuity.
Injection of a solution of iodine (tincture of iodine 1 pt., iodide of
potassium 1 pt., boiled water 20 pts.) has been employed sometimes
with success, but in other cases it has roused a fatal inflammation. It
is best adapted to a simple morbid, relaxed state of the peritoneum.
Saline purgatives (sulphate of soda or magnesia) are especially
useful in constipated cases and should be pushed in continuous
action, as far as the strength of the animal will warrant. By depletion
from the portal system they oppose the tendency to mechanical
transudation, while by rendering the portal blood more dense they
strongly solicit endosmosis from the adjacent peritoneum.
Diuretics have been used extensively and with benefit. They may
prove injurious in a kidney that is already the seat of irritation and
yet after all be the least of two evils. In some cases instead, the
resulting dilution of a dense and irritating urine is directly soothing
to the tender kidney. Saltpeter (10 to 15 grs.), acetate of soda (15 to
30 grs.), squills (1 to 2 scr.), may be repeated so as to keep up a free
action. Pilocarpine (subcutem) (¹⁄₁₀₆ to ¹⁄₃₀ gr. daily), has removed
the ascitic fluid in 14 days (Zahn), but its action is always to be
dreaded in a weak system, or with a diseased heart, or lungs.
A supporting bandage on the abdomen is always useful as
counteracting the tendency to vacuity and further transudation.
A course of bitters and iron, and a supporting diet, and out door
life (sunshine) are important elements in treatment.
 DISEASES OF THE LIVER.
In veterinary and medical works the diseases of the liver have been
accorded a minor place, ill in keeping with the great physiological
importance of the organ. If the function of the liver were
circumscribed by the mere secretion of bile there would be some
excuse for the apparent neglect, as the gland is so deeply situated and
so much enveloped in surrounding organs that physical exploration
is difficult and somewhat unsatisfactory, and the one symptom of
jaundice was long relied on as indicating hepatic disorder.
Taking into account all the varied functions of the liver we realize
the wide-reaching nature of its physiological influence and the
extensive and varied effect of its disorders. We can also deduce, with
greater or lesser certainty, the existence of hepatic disorders from the
morbid conditions of the blood or of organs, the functions of which
are inter-dependent with those of the liver. To elucidate the subject it
is well to trace some of the most prominent functions of the liver; the
following considerations are submitted.
 SANGUIFICATION IN THE LIVER.

Glycogenic function. Glycogen derived through glucose and laevulose from

starch, glycerine, milk and cane sugars. Less from proteids. Peptones as a source.
Its use in cell growth and heat production, in white blood cells, in contracting
muscle, becoming lactic acid. Excess dissolves red globules, setting free
hæmoglobin. Ammonia carbonate and asparagin increases it. Arsenic, phosphorus
or antimony arrests glycogenesis. Liver increases leucocytes, and reduces size of
red globules. Reduction of proteids. Fibrine formers reduced, urea formed; liver
inactivity means less of soluble urea, and more of less soluble and more dangerous
products. Urea increases with hepatic circulation. Hepatic disorder and
suppression of urine dangerous. Red globules probably destroyed. Bile: Amount,
uses, oil solvent, helps endosmosis, deodorant, stimulates glycogenesis, excretory.
Source of bile pigments, tests. Bile acids, dissolve blood globules, antiseptic, tests.
Bile increased by; bile absorbed from bowel, olive oil, salol, salicylates, benzoic
acid and benzoates, turpentine, terpene, terpinol, euonymus, alkalies, arsenic,
ether. Agents lessening biliary secretion, starvation, excess of fat, alkaline iodides,
atropia, strychnia, hepatic diseases, septic duodenal fermentation. Arrest in liver of
copper, iron, iodides, bromides, nicotine, quinine, morphia, curare, toxic bile
products, ptomaines, toxins. Reduces toxicity of peptones, casein, ammonia salts,
indol, phenol.

The liver is the goal to which most of the products of gastric and
intestinal digestion are carried by the portal vein. In the hepatic cells
large quantities of glycogen, 6 (C6H10O5) + H2O, are stored up after
each meal. This is believed to be derived largely from the
transformation of glucose, (C6H12O6) and laevulose (C6H12O6) which
have been produced from starch in the alimentary canal and
conveyed by the portal vein to the liver. By the liberal use of starch,
glycerine, or the sugars of milk, fruit or cane, (but not mannite, or
glycol, or inosite) the glycogen is very greatly increased (to 12 per
cent. in the fowl), but it is diminished on a purely albuminous diet.
Yet it can be produced from albuminous food, as it is always
increased in the dog after a meal of flesh, and is largely present in the
livers of carnivorous animals that have been fed for a month on flesh
only (Landois). The peptones are therefore decomposed in the liver
with the production of glycogen and such waste products as leucin
and tyrosin, which are finally resolved into urea. A purely fatty diet
diminishes it enormously and during prolonged abstinence it
practically disappears. It passes, not into the bile, but into the
hepatic veins, and the general circulation, where it serves in its
decomposition to generate heat, and probably to hasten cell growth.
In the vegetable and animal world, in the germinating seed, and in
cartilage, muscle and epidermis of the fœtus and in the amnios,
glycogen and glucose are found in abundance. The liver, too, the
great center for the production of glycogen, is relatively much larger
in the young and growing animal, and also in the adult animal which
has great power of assimilation.
Glycogen is always present in the white blood globules so long as
they maintain their vitality and amœboid movements, but when they
die, it is replaced by sugar (Hoppe-Seyler). The red blood globules
give up a ferment which rapidly transforms glycogen into sugar.
Glycogen and sugar are evidently of use in muscular contraction as
they are always diminished in the vessels of contracting muscles
(Sanderson), being converted into lactic acid (Bernard).
Forced muscular movements soon expel glycogen from the dog’s
liver, passing it into the blood, and there the excess of glycogen
dissolves the red blood globules. If glycogen is injected into the
blood, achrodextrin and hæmaglobin appear in the urine (Landois).
Ammonia carbonate and asparagin, or glycin, with a carbhydrate
diet produced in rabbits a considerable increase of glycogen
(Rohmann).
Poisoning by arsenic, phosphorus or antimony destroys the
glycogenic function of the liver, which then fails to respond even to
diabetic puncture of the medulla.
There are important changes effected in the blood globules in
passing through the liver. The leucocytes are increased, the hepatic
veins containing 5 or even 10 times as many as the portal vein
(Bernard, Lehmann, McDonald). Their ratio to the red globules is in
the portal vein 1:524 and in the hepatic veins 1:136 (Hirt). The red
globules undergo marked changes, having, in the hepatic veins, a
smaller size, sharper outlines, less flattening in the disc, a habit of
massing together irregularly in place of adhering in rouleaux, and
they dissolve less readily in water.
 REDUCTION OF ALBUMINOIDS.

A large proportion of the fibrine formers are changed in passing

through the liver (Lehmann, Bernard), in man as much as 2,690
grammes daily (Brown Sequard), a fact which goes to account for the
increase of fibrine in inflammation when the liver is inactive. The
change consists mainly in deoxidation and reduction into simpler
compounds which can be more readily dissolved and eliminated.
Arrest of the liver functions in fever is therefore liable to throw into
the blood, products that are little soluble and often poisonous. The
end product is largely urea, and this Cyon always found in excess in
the hepatic veins of dogs (in the portal veins 0.08 grammes, and in
the hepatic veins 0.14 to 0.17 grammes). In man hepatic disorder is
at once marked by the lessening or disappearance of urea from the
urine, and the increase of the less oxidized uric acid (Parkes). In
acute atrophy of the liver, urea disappears from the urine, being
replaced by the less oxidized leucin and tyrosin (Frerichs,
Murchison). In birds urea is replaced by uric acid and this is always
found in the liver.
The increase of urea and allied products bears a direct relation to
the activity of the hepatic circulation. Stimulation of the liver by
electric current sent through the abdominal walls largely increased
the secretion of urea (Sigrist, Stolnikow, Schröder and Salomon).
Murchison, Perrin and Bruardel had a great increase of urea by
stimulating the circulation in the liver. Certain agents ingested are
transformed into urea, among which may be named glycocolle,
brucin, asparagin, sarcine, alanine, and ammonia muriate.
Any degeneration of the hepatic cells which impairs or arrests their
functions lessens the production of urea. In fevers therefore and in
hepatic degenerations the extent of the functional or structural
derangement may be to a large extent gauged by the diminution of
urea. A simple hyperæmia, without as yet any serious impairment of
structure or function, may be attended by a marked increase of urea,
whereas any destruction of the liver cells, or any serious modification
which interferes with the normal function, brings about a decided
decrease. A hepatic disorder accompanied by suppression of urine is
always a grave disorder. On the contrary a free secretion of urine
during liver disease is a favorable symptom.
There is reason to believe that red blood globules are destroyed in
the healthy liver, producing bilirubin and urea (Landois). In diseased
states this becomes excessive, and the resulting coloring matter is
often modified, giving the strong tints, seen in the urine in fever and
certain hepatic disorders.
 SECRETION OF BILE.
The secretion of bile is but a small part of the function of the liver,
and that is by no means a purely eliminating process. Man secretes
in twenty-four hours about 10 parts per 1,000 of body weight, the
dog 14 to 15, the cat 15 to 20, the sheep 25, the rabbit 130, the
Guinea-pig 170, the goose 12 (Cadeac), the horse 12 (Colin). But the
amount varies largely; Scott found that a dog yielded 21, and Kölliker
that another yielded 36 per 1,000 of the body weight.
Only about one-fourth of the biliary acids (Bischoff, Voigt), and
one-eighth of the sulphur (Bidder and Schmidt) of the bile can be
found in the fæces. Most of the bile is re-absorbed from the intestine
and secreted anew, so that, in the course of twenty-four hours, the
material secreted serves the same purpose again and again. During
this repetition of secretion and absorption, it becomes little by little
metamorphosed into other products, which are eliminated by the
lungs and kidneys (Parkes, Murchison).
The functions of the bile so far as known are:
a. The solution of alimentary matters, and especially of fat, in the
intestine, and the hastening of endosmosis, of fats and peptones;
b. The stimulation of peristalsis in the bowel;
c. Antisepsis and deodorization of the contents of the bowels;
d. The determination of the formation of glycogen;
e. The excretion of bile coloring matter, bile acids and cholesterine.
In regard to the glycogenic action it may be said that in cats, the
bile ducts of which have been tied, no glycogen was formed, even
when the diabetic puncture of the brain was made (Legg). Clinical
observation seems to throw some doubt on the formation of bile
coloring matter apart from the liver. In diseased liver with
suspended secretion of bile (waxy and fatty degeneration, cancer,
cirrhosis) the bile pigment was found in neither blood nor urine
(Frerichs, Murchison, Haspell, Budd). Even after extirpation of the
liver in frogs, neither biliary acid nor pigment could be found in the
blood (Müller, Lehmann, Moleschott). These results must, however,
be qualified by the observations of Hammersten who found bilirubin
as a normal constituent of blood serum in the horse, and by
Virchow’s discovery that hæmatoidin (now held to be identical with
bilirubin) is constantly found in old blood extravasations into the
tissues.
The origin of the bile coloring matters may be traced in part to
destruction of red globules in the liver. Quincke has shown that in
the hepatic capillaries in post-embryonic life the leucocytes englobe
and destroy the old and worn out red blood corpuscles which thus
become a source of bile coloring matter. Such destruction is specially
likely to occur in badly maintained conditions of the blood, and in
hepatitis or other liver disease in which the white cells accumulate in
the hepatic capillaries, and when the blood current is retarded.
Hence the liability to jaundice in such conditions. The formation of
new red blood corpuscles has been observed in the protoplasmic cells
of the liver in the embryo, but this has not been established for post-
embryonic life (Neumann, Lowit).
The two common coloring matters of the bile are bilirubin which
colors the yellow bile of man, omnivora, and carnivora and
biliverdin which tints the dark green bile of herbivora. Bilirubin
(C32H36N4O6) forms transparent fox red clinorhombic prisms. It is
insoluble in water but soluble in chloroform, and may thus be
separated from the biliverdin which is insoluble in chloroform.
United as a second basic acid with alkalies it is soluble in water. It is
easily obtained from the red gall-stones of man or ox, and is
chemically identical with hæmatoidin. Biliverdin (C32H36N4O8) is
an oxidized derivative of bilirubin and is insoluble in chloroform,
slightly soluble in ether and freely soluble in water. In addition to its
presence in bile it has been found in the placenta of the bitch. The
test for bile coloring matter is made by placing a drop of the
suspected liquid on a white porcelain plate and adding a drop of
impure, brown, nitric acid (nitric and nitrous acids). If bile is present
there is produced a beautiful play of colors passing from the green of
biliverdin, through blue, violet, red, and ending in yellow.
With regard to the formation of bile pigments in morbid
conditions it may be noted, that agents which dissolve the red blood
globules (such as bile acids or water), when injected into the veins
determine the appearance of bile pigment in the urine (Frerichs,
Kuhne). When we consider that an animal (dog) secretes ¹⁄₅₀ of its
body weight daily of bile, and that nearly all of this is re-absorbed
from the intestines, we can realize this as an important source of bile
and urinary pigments.
Of the bile acids, taurocholic is the most abundant in the bile of
man, birds, and of many mammals and amphibians, while
glycocholic acid is the more plentiful in the ox and pig. It is absent
in sucklings. The taurocholic acid has been found to prove most
destructive to red blood corpuscles, and in strong solution is
distinctly antiseptic, checking the development of bacteria, of the
alcoholic and lactic fermentations and of the tryptic and diastatic
action of pancreatic juice.
These are conjugate acids, formed by the union of cholic acid with
taurin and glycin respectively, and they are found almost exclusively,
in combination with soda in the bile. They are found in the liver and
do not accumulate in the blood when the liver has been removed.
They increase under an albuminous diet.
The test for bile acid, is to take the suspected liquid from which
all albumen has been precipitated, add a few drops of solution of
cane sugar, shake into a froth, and pour sulphuric acid, drop by drop,
down the side of the test tube. A reddish purple color appears in the
froth, and shows two absorption bands at E and F. Any albumen left
in the liquid will give the same color, but only one absorption band.
The secretion of bile is more abundant on animal than on
vegetable food, and on albuminous than fatty. It ceases during
hunger, but is increased by ingestion of water. Its solids are most
abundant one hour after feeding. It increases under a copious and
rapid blood supply, but is arrested by diminished blood flow, even
under increased pressure (in ligature of the vena cava in front of the
diaphragm). Vigorous exertion, drawing off blood to the muscles of
the trunk, diminishes the secretion of bile, while transfusion of
blood, up to a given grade of blood pressure increases it. Nervous
conditions, which cause contraction of the portal vessels, increase
the secretion by forcing more blood through the liver. Such are
strychnia or other stimulation of the valve of Vieussens, of the
inferior cervical ganglion, of the hepatic or splanchnic nerves, or of
the spinal cord. Fever causes its arrest.
The secretion of bile is further stimulated by the following :