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Cha pt er 8: H om e a n d A u t om obi le I n su r a n ce

1
U
2 3
N I N S U R A N C E C O M P A N Y
E I
4 5
G N C L A I M
6
L S N H
7
I U A S S I G N E D R I S K P O O L
G R U M
8
E E R C E
9
N D E O U O
10
C M D V F M W
11 12 13
E N D O R S E M E N T P E R I L B N H
14
T M R N R E O
15 16
O I N S U R E R A A E P R U
17
R D G N P L R S S
18
I D E D U C T I B L E C O L O I E
S C I L A P N H
19
T H A Z A R D A I P E S O
S L L C O R U L
20 21
P E R S O N A L P R O P E R T Y F L O A T E R D
R E A E H I Y A I
O P Y S O C D N N
22
T L M P L Y A C L V
23
E A E N O D M E I E
C C N O N E A A N
24
T E T F S R I S K G B T
25 26
A C V I M S A I E I O
O O E C U B L L R
27
L N N B O D I L Y I N J U R Y L I A B I L I T Y
L T V T L A T
I V E S I B Y
S A R Y T I
I L A S Y L
28
O U G T L P R E M I U M
29
I N S U R A N C E E E A T
30
M W P O L I C Y

Across
3. A risk-sharing firm that assumes financial responsibility for losses that
may result from an insured risk.
4. A request for payment to cover financial losses.
7. Consists of people who are unable to obtain automobile insurance due
to poor driving or accident records and must obtain coverage at high
rates through a state program that requires insurance companies to
accept some of them.
11. An addition of coverage to a standard insurance policy.
12. The cause of a possible loss.
15. An insurance company.
18. The set amount that the policyholder must pay per loss on an insurance
policy.
19. A factor that increases the likelihood of loss through some peril.
20. Additional property insurance to cover the damage or loss of a specific
item of high value.
24. Chance or uncertainty of loss; also used to mean "the insured."
25. A claim settlement in which the insured receives payment based on the
current replacement cost of a damaged or lost item, less depreciation.
(abbreviation)
27. Coverage for the risk of financial loss due to legal expenses, medical
costs, lost wages, and other expenses associated with injuries caused
by an automobile accident for which the insured was responsible.
28. The amount of money a policyholder is charged for an insurance policy.
29. Protection against possible financial loss.
30. A written contract for insurance.
Down
1. Automobile insurance coverage for the cost of injuries to a person and
members of his or her family caused by a driver with inadequate
insurance or by a hit-and-run driver.
2. Failure to take ordinary or reasonable care in a situation.
5. A person covred by an insurance policy.
6. Coverage for a place of residence and its associated financial risks.
8. The protection provided by the terms of an insurance policy.
9. Supplementary personal liability coverage; also called a "personal
catastrophe policy."
10. State legislation that requires drivers to prove their ability to cover the
cost of damage or injury caused by an automobile accident.
13. A list or other documentation of personal belongings, with purchase
dates a cost information.
14. Home or automobile insurance that pays the cost of medical expenses
for people injured on one's property on in one's car.
16. Automobile insurance coverage that protects a person against financial
loss when that person damages the property of others.
17. A person who owns an insurance policy.
21. A claim settlement method in which the insured receives the full cost of
repairing or replacing a damaged or lost item.
22. Legal responsibility for the financial cost of another person's losses or
injuries.
23. An automobile insurance program in which dirvers involved in accidents
collect medical expenses, lost wages, and related injury costs from their
own insurance companies.
26. Automobile insurance that pays for damage to the insured's car when it
is involved in an accident.
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minute) and respirations (6 per minute) in connection with a mild
peritonitis, intestinal catarrh, colicy pains and diarrhœa. The
conjunctiva is pale, the pulse compressible, the respirations unequal
and accompanied by a moan, and the appetite impaired or lost.
If confined to mere spots on the liver, a restoration to apparently
vigorous health may take place, but if extensive it may lead to
compression and obstruction of the portal vein or bile duct, or to
compression and atrophy of the liver, with corresponding symptoms.
Treatment. As in other congestions of the liver, the use of salines
to deplete the portal system, and of alkaline diuretics are especially
indicated, to be followed by bitters and mineral acids. Sinapisms and
other counter-irritants to the region of the liver are of great service.
If not complicated with abscess, or microbian infection, cases of this
kind will often do well.
 CIRRHOSIS OF THE LIVER. FIBROID
DEGENERATION.

Definition. Increase of connective tissue, decrease of gland parenchyma. Causes:

in man, alcoholism; in animals, chronic heart disease, chronic recurrent
perihepatitis, biliary obstruction, toxins. In horses: age, emphysema, unwholesome
fodders, vegetable alkaloids, infection. Symptoms: prostration, hebetude, impaired
appetite, colics, constipation, later diarrhœa, unthriftiness, emaciation, dropsy,
icterus, ascites, intestinal catarrh, tender hypochondrium, early fatigue. Lesions:
increase of connective tissue, compression and absorption of parenchymatous
tissue, greatest around portal vessels, thickening of fibrous stroma between
capillaries of acini, shrunken, granular, pigmented liver cells. Treatment: salines,
Glauber salts, diuretics, sodium carbonate, or iodide, or salicylate, derivatives,
mineral acids, bitters, open air, laxative food, pure water. In cattle: obstruction to
circulation or the flow of bile; advances from the vessels, causes absorption,
caseated foci, adhesions, enlarged liver. Symptoms: jaundice, yellow, red,
albuminous urine, chronic indigestion, tends to fatal though slow advance.
Treatment: green food, open air life, saline laxatives, alkalies. In dog: common
following heart disease, parasites, bacteria. Lesions: Congested brownish red liver,
fibroid increase from Glisson’s capsule, compression of acini, their elevation above
surface, fatty and pigmentary degeneration of hepatic cells, increasing sclerosis.
Symptoms: as in parenchymatous hepatitis with slower advance, in time tender
loins, brownish or reddish urine, ascites, intestinal catarrh, it may be icterus.
Treatment: Correct cardiac troubles, digitalis, strophanthus, and intestinal, careful
diet, mineral acids, bitters, pure water, saline laxatives, antiseptics, alkaline
diuretics. Potassium iodide. Derivatives. Draw off liquid. Laxative non-stimulating
diet.

Definition. An interstitial inflammation of the liver characterized

by a great increase of the connective tissue and compression, atrophy
and degeneration of the glandular elements.
The same final result may undoubtedly originate in various
different primary morbid processes.
 In man cirrhosis is looked upon as almost always the result of
abuse of alcohol. In animals this cannot be the case, apart from a few
kept in connection with breweries or distilleries.
In heart disease a long continued mechanical congestion of the
liver causes compression and degeneration of the secreting cells in
the centre of the acini (around the intralobular veins), while the
peripheral portions undergo cell proliferation and increase of
connective tissue.
In chronic or recurrent perihepatitis, a whole lobe may be
compressed by the hyperplasia of the investing connective tissue,
and the hepatic cells are degenerated and absorbed.
Overdistension of the biliary ducts from obstruction to the flow of
bile (gall stone, catarrhal inflammation, constipation), leads to
proliferation and hyperplasia in the walls of the biliary radicals
throughout the entire liver.
The presence in the liver of toxic agents, ingested, or generated
from microbian fermentation in the intestinal canal or liver is
another recognized cause of connective tissue hyperplasia.
 CIRRHOSIS IN THE HORSE.
Cirrhosis of venous origin has been observed mainly in old horses,
while hypertrophic cirrhosis from biliary obstruction occurs rather in
the young (Cadeac). Bruckmüller records a case of the first kind in a
horse with extreme pulmonary emphysema. Walley gives a bad
condition of fodders as the main cause, virtually implying, in many
cases, infective catarrh and obstruction of the biliary ducts.
A form of the disease prevails at Schweinsberg in Hesse, and has
been variously attributed to spoiled fodders (Nicklas), to vegetable
alkaloids and other poisons in the food (Friedberger and Fröhner), to
clover, to telluric poisons (Redner), to infection (Meminger), and to
heredity (Neidhardt). It is a suggestive fact that it is confined to the
valleys of the Ohm, Glon, and Zusam where the land is peaty or
swampy and subject to inundations, while it is unknown on the dry
table lands (Friedberger and Fröhner). This strongly suggests
intoxication with microbes or their deleterious products. The gastric
catarrh that frequently attends the disease may point in the same
direction.
Symptoms. These are too often general rather than diagnostic.
Dullness, prostration, hebetude, yawning, hot, sticky mouth, lost,
irregular or depraved appetite, colics, constipation or diarrhœa, dry,
harsh coat, emaciation, weakness, œdema of the limbs, vertigo and
drowsiness may be among the symptoms. More characteristic are
icterus, abdominal distension from ascites, or congestion of the liver,
yellow or high colored urine, intestinal catarrh, indigestion, and
tenderness in the region of the liver. The mucosæ are usually pale at
first and not always icteric later. On exertion the horse shows early
fatigue, tumultuous heart beats and oppressed breathing.
The Schweinsberg disease often lasts for months, with alternate
improvements and exacerbations, but almost invariably ends in
death, and sometimes completely depopulates a stable.
Lesions. These consist primarily in the great increase of the
connective tissue and the relative decrease of the hepatic tissue. This
is usually mostly around the divisions of the portal vein and the
periphery of the acini, but also in the end around the hepatic veins as
well. When it has formed around the biliary canals there is a great
increase of the liver (often doubled) and its edges have become
rounded. Within the acini the increase of the fibrous stroma is seen
between the radiating capillaries, and the hepatic cells are
contracted, granular, pigmented, and comparatively destitute of
protoplasm around the still persistent nucleus.
Treatment. Glauber salts to clear the bowels of offensive matter,
and deplete from liver and portal vein, bicarbonate of soda or iodide
of potassium to eliminate the poisons through the kidneys and to
lessen the induration, and finally salicylate of soda as a liver
stimulant and intestinal antiseptic are suggestive of the line of
treatment that may be pursued. The saline laxatives and diuretics,
and antiseptics may be changed for others according to special
indications, and bitters and mineral acids may be resorted to.
Counter-irritants to the right hypochondrium should not be
neglected in case of local tenderness. In the otherwise fatal
Schweinsberg disease, Imminger, Künke and Stenert had a
remarkable success from the free use of potassium iodide, which
suggests a cryptogamic origin, as this agent is so valuable in polyuria
which results from musty fodder. In all cases, gentle exercise in the
open air and a moderate ration of laxative food (green) are of great
value. Above all the old suspected diet should be carefully avoided,
also any impure water supply.
 CIRRHOSIS IN CATTLE.

This has been recorded by different observers and usually as the

result of some obstacle to the circulation, or of catarrh and
obstruction of the biliary passages. Morot saw it in young calves,
which showed greatly enlarged liver (in one case 24 lbs.) and
kidneys, the former containing numerous cysts and marked sclerous
thickening around the vessels. This advancing thickening of the
connective tissue, causes increasing firmness of the liver and
absorption, distortion and diminution of the lobules. Albrecht
describes a chronic interstitial hepatitis with caseated centres
(nontuberculous) many of them an inch in diameter. The liver is
brown or grayish with whiter callosities which extend into its
substance and make points of attachment to the diaphragm or other
adjacent organ. The contrast between the fibrous layers and the
hepatic tissue has been likened to a checker board (Höhmann). The
enlarged liver may weigh 30 lbs.; in one remarkable case it weighed
300 lbs. (Adam). The bile is of a light color and mixed with mucus.
Symptoms. The symptoms are indefinite: a gradually increasing
jaundice, the passage of yellowish red urine becoming more and
more red and albuminous, and finally coagulating on the walls of the
urethra or on the litter, chronic indigestion, salivation (Schäffer),
weakness, breathlessness and more or less fever may give indications
of the disorder. Höhmann failed to find tenderness of the right
hypochondrium. The disease is liable to go on to a fatal issue, so that
it is often sought to prepare the animal for the butcher.
Treatment will follow the same line as in the horse. Green food,
pasturage, open air life, saline laxatives, and alkalies with a free use
of potassium iodide to check the sclerosis will be indicated.
 CIRRHOSIS IN THE DOG.

In the dog, cirrhosis is much more common than in the larger

animals, in connection with idle pampered habits, the frequency of
diseased heart and consequent disturbance of the circulation, and
the presence of parasites in the liver or biliary ducts. Bacteria
intoxication and infection are also common.
Lesions. The liver is at first tumefied, with hard consistency and
rounded edges, and a deep brownish red color, but this is modified
by the grayish fibroid hyperplasia which is especially abundant in
and around the vaginal sheaths of the capsule of Glisson. In cases
arising from diseased right heart or lungs the induration is rather
concentrated around the hepatic veins. The contraction and
shrinking of the fibroid hyperplasia as the disease advances causes
the projection of the hepatic tissue in minute rounded elevations
which give a peculiar uneven appearance to the surface of the organ.
The fibroid growth gives a remarkable hardness to the liver which
resists even the edge of a knife. The hepatic cells are the seat of fatty
and pigmentary degeneration. Inflammation and tumefaction of the
kidneys, and ascites are common features of the malady.
Symptoms. The general symptoms are as in parenchymatous
hepatitis with a more tardy development. There are impaired or
irregular appetite, dullness, sluggishness, in an obese animal short-
windedness or palpitations on slight exertion, symptoms of disease
of the heart, lungs or digestive organs, a spasmodic cough,
constipation followed by relaxation of the bowels, nausea and
vomiting. As the disease advances tenderness of the loins, the
passage of brownish or reddish, albuminous urine, the formation of
ascites and of gastro-intestinal catarrh may be noticed. Icterus may
be entirely absent, but, with a flaccid abdomen, enlarged liver and
spleen may be detected.
 Treatment. The indications are to first combat the causes.
Irregularities in the heart’s action may be met by digitalis or
strophanthus; gastro-intestinal catarrh by a carefully regulated diet,
with mineral acids and bitters; portal congestion by a free use of
water and other diluents and by saline laxatives; intestinal
fermentations by antiferments (salol, naphthol) and toxic matters in
the blood by alkaline diuretics. For the liver hyperplasia, potassium
iodide may be freely used. Blisters to the right side will occasionally
prove useful. The ascitic fluid must be drawn off when it
accumulates. A diet of milk, bread and milk, buttermilk and mush, or
one in which albuminoid elements are in minimum amount and the
action of which is laxative is to be preferred. Out door exercise is
desirable.
 CHRONIC ATROPHY OF THE LIVER.
Chronic Atrophy: In old horses: in right and spigelian lobes; others show
hypertrophy. In ruminants, omnivora and carnivora: in areas compressed by
tumors or parasites. Perihepatitis. Sclerosis. Remedy causes if possible. Fatty
Degeneration: Oil globules in liver cells, pathological when they destroy the
protoplasm. In ducks and geese on forced feeding. Causes: poisoning by
phosphorus, arsenic, antimony, lead, phenol, iodoform, alcohol; excess of fat in
food, spoiled fodders, colchicum autumnale, yellow lupins, bacteria, hemorrhages,
inflammations, tumors, parasites; improved meat producing breeds, old animals,
hot stables. Lesions: liver enlarged, pale, yellow, bloodless, knife in cutting is
smeared with fat, oily stain on paper, liver cells enlarged, protoplasm replaced by
fat or oil; may be circumscribed. Symptoms: obesity, over-fed in fats and starches,
of fattening breed, kept in confinement, in hot moist environment, if fed certain
poisons, with costiveness and indigestion, no endurance, short winded, slight
icterus, scanty urine, little urea, later, emaciation, palpation of enlarged liver.
Treatment: send to butcher, pampered horses, cows from swill stable, a run at
grass, with shade trees, a poor pasture, salines, cholagogues, mineral acids, bitters,
iron with alkalies, currying, massage, douches.
Acute yellow atrophy has been referred to under parenchymatous
hepatitis but a chronic atrophy is also met with in all domestic
animals.
In old horses it affects, by preference the right and spigelian lobes,
the portal circulation of which is less direct because of the veins of
supply leaving the parent trunk at right angles (Leblanc), and
because these lobes are more exposed to compression by solid
accumulations in the double colon (Kitt). In such cases a
compensatory hypertrophy of the left and middle lobes is often
observed.
In ruminants the lesion is often circumscribed to the areas that
have undergone compression by tumors or parasites (echinococcus,
actinomycosis), and there may be compensatory increase elsewhere
in the organ.
In swine, dogs and cats the same conditions are operative. In all
alike perihepatitis may be a causative factor, and sclerosis (cirrhosis),
with contraction of the fibrous hyperplasia may also operate.
 Symptoms are very obscure and treatment unsatisfactory unless
the active causes can be recognized and arrested.
HEPATIC STEATOSIS. FATTY LIVER. FATTY
DEGENERATION.
The presence of oil globules in the liver cells is normal and
physiological, the liver acting to a certain extent as a store-house for
fat. This is always a marked feature, in healthy animals on high
rations, and taking little or no work, but so long as the protoplasm
and nuclei of the cells retain the normal characters and functions the
condition is not a morbid one. It may, however, become excessive,
with great enlargement of the liver, and with the substitution of fatty
granules for the protoplasm of the cells as in ducks and geese
subjected to forced feeding, and the condition becomes a distinctly
pathological one.
In true fatty degeneration the protoplasm of the hepatic cells is
destroyed and replaced by fatty granules, the resulting condition
being a permanent destruction of the cell for physiological uses.
Causes. The liver cells undergo fatty degeneration under the action
of certain poisons like phosphorus, arsenic, antimony, lead, phenol,
iodoform and alcohol. According to Neyraud oxide of antimony is
given daily to fattening geese to hasten the development of fatty liver.
An excess of fatty elements in the food leads to the same result as
shown first by Majendie in dogs, in which not only did the liver
undergo this degeneration but the sebaceous glands of the skin
secreted an excess of volatile fatty acids.
The cryptogams and their products on musty fodders determine a
gastro-enteritis in herbivora, accompanied by fatty degeneration of
the liver.
Colchicum Autumnale, and poisonous yellow lupin both determine
this degeneration.
The products of a number of pathogenic bacteria have a similar
effect. This has been noticed in the cat with bacillus pyocyaneus
(Charrin), the cholera spirillum, pyæmic and septicæmic infection,
contagious pneumonia of the horse, strangles, and ulcerative
endocarditis. It has been long noticed to be a complication of
pulmonary tuberculosis, the result in this as in other affections of the
lungs having been attributed to lessened oxidation in the tissues. It
occurs also in hæmorrhages, ruptures and inflammations of the liver
and in passive congestions of the organ, the impairment of the
normal functions (in the altered conditions of nutrition, or under the
influence of poisons,) proving an important factor in the process. The
same remark may apply to the fatty degeneration which complicates
most other liver diseases, cirrhosis, catarrh of the bile ducts,
distomatosis, echinococcus, carcinoma, and epithelioma.
Certain other factors must be taken into account. The inherited
disposition to the production of fat which characterizes the improved
breeds of butcher animals, and particular individuals of all breeds,
mature age which predisposes to the deposit of fat in internal organs,
old age which lessens the vitality of the cells, and hot, damp climates
or stables, all operate more or less in determining the fatty change.
Lesions. In fatty degeneration the liver is enlarged, pale, bloodless,
yellowish, its cut surface exudes an oily fluid which smears the knife,
and it is so light that it floats on water. If scraped and the material
drawn across a sheet of paper it forms a transparent oily stain. Under
the microscope the liver cells are seen to be enlarged and to have
their protoplasm and nuclei replaced by fat or oil. If due to
obstruction in the heart or lungs the degeneration is greatest toward
the centre of the acinus, if due to an infectious disease it is usually
greatest towards its periphery. In infectious diseases too the liver is
not pale yellow, but usually of a deep brownish or yellowish red. The
degeneration may be local or general. McFadyean found a
circumscribed lesion in an ox’s liver, of a bright ochreous color, and
the cells completely transformed into fat cells, while the rest of the
liver was sound. In the dog fatty areas, up to an inch in diameter, are
not uncommon. The swollen cells pressing on the adjacent vessels,
account for the bloodless condition, and favor the degenerative
process.
Neyraud records a fatty liver of 28 ℔s. weight from the horse, and
Kitt one of 10 ℔s. from the pig.
Symptoms. Like as in most chronic liver diseases the indications
are uncertain. The conditions may, however, suggest fatty
degeneration; if the patient is very obese; if it has had an abundant
food, rich in hydrocarbons and carbohydrates, and little exercise; if it
has received in food or water continuous doses of phosphorus,
arsenic or antimony; if it has lived in a hot moist climate or stable; if
there has been a tendency to costiveness and indigestion; if the
patient is weak, easily fatigued and short-winded; if there is a slightly
yellowish red tinge of the conjunctiva and if the urine is scanty and
contains little urea. If the disease is more advanced and the animal
emaciated, it may be possible in the smaller animals at least to
manipulate the liver to make out its increase, its smooth surface, and
its absence of tenderness.
Treatment. When met with in meat producing animals the best
resort is to turn these over to the butcher. When in an animal which
is mainly valuable for breeding purposes, or in horses or carnivora,
something may be done to check the progress of the malady, and
maintain at least the present condition. The value of this will of
course depend on how far the disease has already progressed. Cows
that have spent a winter in a hot swill stable are of little use
afterward for breeding or dairy uses and advanced cases of fatty
degeneration in the horse or dog hold out little hope of a satisfactory
issue. For cases in the earlier stages, nothing can be better than a run
at grass, where there is opportunity for shelter from the noonday
sun. If the pasture is short and the animal has to exercise to secure a
living, so much the better. If kept indoors the patient should have a
clean, roomy airy box stall, with a moderate allowance of easily
digested food, and laxatives and cholagogues daily such as Glauber
salts, aloes, calomel, podophyllin or cream of tartar. Mineral acids,
especially nitro-muriatic acid, and bitters may also be given. The
preparations of iron are sometimes useful in maintaining the tone of
the digestive organs and counteracting anæmia but they must be
conjoined with diuretic doses of bicarbonate of soda.
There is great advantage in stimulating the skin, and active
brushing, currying, hand-rubbing, and even cold douches may be
resorted to.
 AMYLOID DEGENERATION OF THE LIVER.
Degeneration of basement substance of connective tissue, swollen, transparent,
homogeneous, colored mahogany brown by iodide. In wasting diseases, tubercle,
cancer, malaria, dysentery, leukæmia, suppuration, ulceration, pleurisy,
pericarditis, peritonitis, chronic catarrh, broncho-pneumonia, orchitis, biliary
calculi, nephritis. Chronic. Lesions: Affected part swollen, sinks in water,
bloodless, clear, smooth, homogeneous, yellowish or reddish gray, under
compound solution of iodine becomes mahogany brown, under sulphuric acid dark
violet. Extends from vessel walls to adjacent connective tissue. Symptoms: Of
wasting diseases, but not diagnostic. Treatment: Unsatisfactory, directed to
causative disease.
This is a condition in which the basement substance of the
connective tissue, and especially of the walls of the vessels, becomes
swollen and composed of a transparent, homogeneous substance,
albuminous in character, and which stains of a deep mahogany
brown on the application of a solution of iodine. The degeneration is
usually associated with severe wasting diseases, in the human being
with tuberculosis, syphilis, malignant tumors, malarial infection,
dysentery, leukæmia, and chronic suppuration or ulceration,
especially of the bones.
In the lower animals (horse, dog, ox, sheep, rabbit, poultry) it has
been seen to attend or follow on similar cachectic conditions. In the
horse it has been seen in connection with the effusions of pleurisy,
pericarditis and peritonitis (Rabe), in chronic bronchial catarrh
(Fischkin), in chronic broncho-pneumonia, and dilated right heart
(Trasbot), in orchitis, phlebitis and cachectic states (Caparini), and
in calculous obstruction of the biliary duct (Burgoin). In cattle it has
accompanied chronic nephritis (Brückmüller), tuberculosis,
leukæmia, etc. In lambs kept in confined stables, though well feed on
oats (Werner). In long standing suppurations and in animals fed on
distillery swill it has been observed.
It may last for months or years, and predispose to other disorders,
functional and structural. It does not, however, interrupt secretion as
bile continues to be formed.
 Lesions. The affected part of the liver is enlarged, the entire organ
in the horse may amount to 32 lbs. It is smooth and even, though
thick and rounded at its inferior border, yet occasionally on the
posterior aspect there may be hyperplasia and a rough irregular
surface. The diseased liver is heavy and sinks in water, unlike the
fatty liver. In the horse it is soft and friable or even pasty whereas in
man it is firm and resistant. The cut surface is bloodless, smooth,
clear, homogeneous and grayish, yellowish or reddish gray. When
treated with a solution of iodine and potassium iodide it changes to a
deep mahogany brown; if dilute sulphuric acid is then used it
changes to a deep violet, almost black color. If the iodine solution is
brushed over the smooth cut surface the mahogany color of the
amyloid stands out in marked contrast with the bright yellow of the
healthy hepatic tissue. The amyloid commences in the walls of the
smallest arteries, in the media and intermediary layers of the intima,
and thickens the walls so as to obstruct their lumen more or less
completely and render the part comparatively exsanguine. It may
extend to the connective tissue of the organ, but it is not certain that
the hepatic cells are involved in the process. The cells are, however,
pressed upon by the diseased vessels and stroma and undergo
consequent fatty degeneration. The amyloid may be confined to but a
small part of the liver or to its smaller blood-vessels or it may extend
to the whole. In fowls it is always in multiple centres (Leisering). It
may be found in other important organs, kidneys, spleen, lymphatic
glands, intestinal mucosa, etc.
Symptoms are not diagnostic. If with an old standing, exhausting
disease, paresis, weakness, emaciation and unfitness for work, there
is loss of appetite, dryness of the mouth, congestion of the rectal
mucosa, yellowish, whitish, or dark tarry fæces, and a slightly
brownish or yellowish tinge of the visible mucous membranes
(Rexante) it may be suspected. In fowls Leisering noticed, weakness,
lameness, ruffling of the feathers and attacks of vertigo. Icterus,
ascites and tenderness over the region of the liver may all be absent.
In the absence of ascites, tympany, or an excess of fat in the smaller
animals, manipulation may detect the considerable enlargement of
the liver, and the characteristic smoothness, of its surface. In other
cases some indication may, at times, be had from the increased area
of dullness on percussion.
 Treatment is essentially unsatisfactory even if a correct diagnosis
can be made. The most hopeful course would be to correct the
debilitating disease in which the amyloid seems to have originated.
Diseased bones, ulcers, chronic suppurations, and catarrhs may be
done away with, and at least any further advance of the degeneration
arrested. Open air exercise and a green or otherwise laxative diet
would be indicated. The amyloid in lambs fed on oats was corrected
by a change of diet (Werner). As medication the alteratives,
potassium iodide and potassium arseniate have been mainly resorted
to. Bitters and iron may also be of use to build up the strength. The
latter should be given with potassium bicarbonate.
 BLACK PIGMENTATION OF THE HEPATIC
CELLS. BROWN ATROPHY.
In horse. With melanoma and atrophy, or without, pigment granules fill hepatic
cells, liver becomes brown or black. In calves. In sheep. Apart from melanosis, the
real cause unknown.
The accumulation of granules of black pigment in the hepatic cells
has been noticed in old and worn out horses (Louis Blanc, Cadeac,
Bruckmüller), in calves (Degive, Cadeac), and in sheep
(Siedamgrotzky, Barrier). In horses it has been found in connection
with atrophy, or in other cases, with melanotic tumors in other parts.
In atrophic cases the liver is small, puckered, brown and dull, with a
leathery appearance on section, and with the hepatic cells charged
with pigment granules so that each acinus has a stellate appearance
from the radiating lines of cells. This constitutes brown atrophy.
The second form which may be called melanotic liver, is not
associated with atrophy, but is characterized by the crowding of the
hepatic cells with black pigment granules, which fill up the
protoplasm and crowd the still pale nucleus to one side. The affected
portions become of a deep black.
In calves the pigmentation may be confined to the superficial
portion of the liver (Degive).
In sheep pigmentation may be in the peripheral cells only of the
acinus (Cadeac) but is about equally distributed on the surface, and
throughout the interior of the liver, and may extend to the stroma of
the gland (Siedamgrotzky).
Apart from the general causes of melanosis, benignant or
malignant, no definite reason for this pigmentation has been
assigned. The development of melanæmia and tissue pigmentation in
man from malarious microörganisms suggests that other germs and
their products may have a similar effect in the lower animals but
nothing certain is known as to the true cause.
Apart from melanosis, it is not known that this pigmentation of the
hepatic cells is of any essential pathological importance. It is
important however for the veterinarian to be acquainted with the
condition, that he may intelligently deal with such lesions whether
seen in ordinary post mortem examinations, or in the course of meat
inspection.
 DILATATION OF THE GALL BLADDER AND
BILE DUCTS.
Causes: obstruction of common bile duct, distoma, round worms, tæmiæ, gall
stones, encrustations, inflammations, tumors, cicatrices, hydatids. Congenital
absence. Ducts stand out on liver. Symptoms of colic, icterus, bile poisoning,
marasmus. Treat the causative conditions.
This may occur in all our domestic animals except solipeds in
which latter there is no gall bladder.
Causes. Any serious obstruction to the discharge of the bile into
the duodenum may cause it. The presence of trematodes, nematodes,
or even tæniæ in the ducts, gall stones, incrustations, occlusion of the
ducts by inflammatory swelling, tumors of the liver or adjacent parts,
echinococcus, cysticercus, or cicatrices may be cited. Cadeac
mentions a case of congenital atresia of the bile duct in the calf.
Vigney records a case in the cow in which the greatly dilated gall
bladder formed a hernial mass in the epigastric region which was,
however, easily reduced by manipulation.
In all such cases the distended bile ducts stand out as white
branching lines on the back of the liver converging toward the portal
fissure. The walls of the ducts may be attenuated or thickened and it
is alleged calcified. They are usually lined by a deposit of cretaceous
consistency precipitated from the retained bile. The contents of the
distended ducts and bladder are variable. They may have the color
(yellow, green) and consistency of bile; they may be thick, dense and
albuminous; they may be thin and serous from inflammatory or
dropsical exudation; they may be granular, or purulent.
Though there is no gall bladder, in the soliped, a similar condition
of the biliary ducts may be produced in the same way.
According to the degree of obstruction there may be more or less
acute symptoms of biliary colic, icterus, marasmus, poisoning by bile
acids, etc.
Treatment must be directed toward the removal of the special
cause of dilatation.
 DOUBLE GALL-BLADDER.
As a congenital formation the gall bladder is sometimes divided
into two at its fundus, and in other cases the division extends
throughout, forming two complete sacs. This has been found in the
sheep, cat, ox (Gurlt, Goubaux) and pig (Goubaux). Such a
redundancy does not interfere with normal functions.