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Note:
written for Beardies, but may be applied to PONS.
Chronic small
intestinal disease is a problem for many beardies.
In young dogs especially, chronic intermittent small
bowel diarrhea often accompanied by weight loss or
failure to gain weight may be the result of
bacterial overgrowth. This isn’t the only
presentation, some dogs may not have diarrhea,
others may vomit or have mild colitis, but in
general they are young and not doing well. Bad
bacteria can become established for a variety of
reasons, but mostly these can be grouped as due to
defective production of stomach acid, defective gut
motility, defective local immunity, exocrine
pancreatic insufficiency, defective mucus
production, unabsorbed nutrients and malnutrition.
Where possible the underlying cause of the problem
should be treated. If this cannot be determined oral
oxytetracycline or tylosin are usually effective
treatments.
Dietary
sensitivity (allergic reaction) and food intolerance
can also cause chronic diarrhea. Usually the two
conditions are difficult to distinguish, and are
treated similarly. Exclusion diets using a protein
and carbohydrate source the dog has not previously
experienced. Owners should never feed any treats
during this phase, just the prescribed diet. It can
take 6 to 8 weeks for an improvement to be seen. At
this point to confirm diagnosis the dog should be
challenged with the original diet – which should
cause problems to reappear (surprisingly many owners
are reluctant to complete this step). Foods should
be reintroduced one item at a time. Unfortunately,
truly allergic dogs develop allergies to the new
ingredients over time. Steroids may help reduce the
allergic response. Raw and home cooked diets may
also prove successful for these dogs, and evidence
of allergy to the grain mites in kibble has recently
been reported.
Infiltration of
the lamina propria of the small intestine wall is
characteristic of inflammatory bowel disease (IBD).
In the most common form the invading cells are
lymphocytes and plasma cells; less commonly the
invading cells are eosinophils. This condition may
also co-occur with dietary sensitivity, bacterial
overgrowth, giardia, campylobacter and
histoplasmosis and other fungal infections as well
as lymphosarcoma. Co-existing problems should be
addressed. Grossly the intestinal wall may appear
normal or thickened, and definitive diagnosis is
made from biopsy samples taken during endoscopic
examination. Treatment is similar to that for
dietary sensitivity. Reducing carbohydrate and/or
replacing other sources with rice can be very
helpful, as can replacing long chain fatty acids
with medium chain ones.
Intestinal
lymphangiectasia is a protein losing condition in
which flow of lymph from the intestines is blocked,
the lymph ducts can rupture and release plasma
proteins into the intestines. It may be congenital
or acquired, most often subsequent to congestive
heart failure. A diet high in good quality protein
and low in fat, supplemented with fat soluble
vitamins is helpful. Steroids may help relieve
clinical signs. Where possible the underlying cause
should be treated.
Adenocarcinoma is
the most common intestinal tumor, although
lymphosarcoma, leiomyoma, leiomyosarcoma,
fibrosarcoma and intestinal polyps can occur. Signs
of these are vague and progress slowly. Anorexia and
weight loss are usually the first signs.
Adenocarcinoma usually occurs in the duodenum or
large intestine, and may spread locally and
sometimes to more distant sites. Mean survival after
surgery is about 7 months. Lymphosarcoma usually
spreads to the lymph nodes and response to
chemotherapy in dogs is poor. Leiomyoma and
leiomyosarcoma are tumors of the muscle wall, and if
you can resect the tumor this is usually curative as
they rarely metastasize.
The Large
Intestine is
between 28 and 90 cms in dogs, and runs from the end
of the ileum to the anus. There are three sections.
The cecum is an 8 to 30 cms. long pouch off the
colon shortly after it leaves the ileum. The colon
has two distinct bends as it passes through the
abdomen to the rectum. The cell layers of the wall
are similar to those of the small intestine;
however, there are no villi and fewer microvilli,
but more mucous secreting cells. Cell turnover here
is slower (4 to 7 days). The large intestine’s
primary function is to extract water and
electrolytes from the effluent from the ileum, and
to store feces prior to defecation. A small amount
of fermentation of organic material occurs in the
first part of the colon, but this is of little
significance, unlike the same process in herbivores.
Most muscle contractions are actually away from the
rectum, slowing down the passage of the contents
while they are mixed, stored and dehydrated. Towards
the anus, spontaneous giant contractions propel the
contents into the rectum. The large bowel has a
limited capacity for removing water. Normally it
removes 90% of the remaining water, but if excess
water comes from the small intestine, it may be
overwhelmed, and the result is diarrhea. Sodium is
also absorbed, and potassium and bicarbonate
secreted. The latter neutralizes acids produced by
fermentation. Bacterial content in the gut is
highest in the large intestine, with 10 11 organisms
in each gram of feces – nearly 50% of its dry
weight. The bacteria resist bacterial overgrowth
with unfriendly bacteria, while metabolizing any
remaining carbohydrates, proteins and lipids.
Diarrhea is the
most common sign of large bowel disease. It is
characterized by a lot of mucous, and often
accompanied by straining. Blood will be red rather
than the black tarry melena seen with small
intestinal bleeding. Frequency of defecation is
increased, but the amount is diminished. Dogs
usually remain bright and normal; weight loss is
uncommon. Strictures or tumors may result in the
production of abnormally shaped feces. Vomiting and
weight loss indicate small intestinal disease is
present too. Diarrhea can be the result of dietary
indiscretion or changing diet too quickly for the
enzymes to adapt; whipworm infection; IBD or
neoplasia. Tumors can be benign – adenoma, leiomyoma
or malignant – adenocarcinoma, lymphosarcoma or
leiomyosarcoma – although the latter can usually be
surgically removed completely. Irritable bowel
syndrome, also called nervous or spastic colon, is a
vague term for large bowel diarrhea that is often
fiber responsive (psyllium is curative) or caused by
toxins produced by clostridial bacteria. Other
causes of large bowel diarrhea are fungal, bacterial
or parasitic.
Constipation may
result from too efficient removal of fluid from the
bowel or insufficient mucous production. Megacolon –
enlargement of the colon leading to poor motility –
is rare in dogs, and is usually acquired secondary
to prolonged mechanical or functional obstruction of
defecation.
Function of the
rectum and anus depends on the coordination of
conscious and unconscious muscular movements. The
rectum begins as the colon enters the pelvis. The
region is rich in mucous secreting cells. If these
cells become inflamed then mucous secretion
increases, as does straining and the presence of
blood in the feces. Three kinds of glands empty into
the anal region. Anal glands are modified sweat
glands that secrete lipid into the lumen of the
anus. The glands of the paired anal sacs that lie at
positions 4 and 8 just below the skin around the
anus secrete a mixture of dead cells, protein,
sebaceous fluid and bacteria into the sacs. The
circumanal glands surround the anus and are
non-secretory. The anus has two sphincters, the
internal one is not under conscious control. The
external sphincter surrounds the internal one, and
is under conscious control. The two sphincters are
normally perfectly coordinated, but damage to the
pudendal nerve can result in fecal incontinence.
While the anus is
not involved in digestion, problems can frequently
result in owners deciding to euthanatize the dog.
Problems in the area can include: perineal hernia –
rectum, urinary bladder or prostate gland can
herniate into the anal region; rectal polyps and
other tumors; rectal prolapse; proctitis –
inflammation often secondary to colitis; rectal
stricture – usually the result of trauma or surgery;
rectal foreign bodies – these may lodge in the
rectum having passed through the rest of the
intestinal tract. Foreign bodies can cause secondary
fistulas and abscesses. Perianal fistulas are
extremely painful and consist of one or multiple
tracts running from the lumen of the anus through
the skin in the region around the anus. Dogs with
broad tail bases that clamp their tails are at
increased risk. Low thyroid and poor immune function
may also be inciting factors. Surgery and/or topical
tacrolimus usually is curative.
Anal sac
impaction, inflammation and/or abscessation is
common, and owners notice their dog licking or
biting at the area, scooting their butts, having
trouble sitting (or showing reluctance to do so),
pain and straining on defecation. One or both sacs
may be involved, and they can readily be palpated
through the skin. Normal secretions are clear to
pale yellowish brown. Granular material, pus, blood
and turbidity are all abnormal. Normally impacted
sacs can be expressed easily, but sometimes the
secretions form a cement-like block which has to be
cleared before you can express them. Abscesses are
extremely painful, and can cause fever. They can
also lead to fistulas forming. In dogs with a
chronic problem, removal of the sacs is recommended.
Feeding a high fiber diet may help express the sacs.
Adenocarcinomas may affect the anal sacs, and
usually metastasize to the nearby lymph nodes.
The Liver carries
out at least 1500 biochemical functions essential to
a dog’s survival. It is involved in the metabolism
of carbohydrates, lipids, protein, vitamins and
endocrine hormones; immune function; storage; making
blood clotting factors, iron regulation and even
making blood in utero and in extreme situations;
making, storing and regulating the secretion of
bile; and the detoxifying and excreting of drugs,
hormones and several other substances. Its storage
capacity, functional reserve and regenerative
capabilities are the stuff of legend, but this
doesn’t make it easy to recognize when something is
amiss; and often disease is severe and advanced
before a problem is detected.
The liver is
composed of six lobes. About 80% of the volume
consists of hepatocytes. Another important cell type
is the Kupffer cell, these line the blood vessels
passing through the liver. These are fixed
macrophages – cells that ingest and detoxify
substances. They are also needed for the metabolism
of iron, lipid, cholesterol and certain hormones. In
addition, they have several important functions in
the immune system. Ito cells are rich in retinoids
and store lipids; they also produce most of the
collagen that results in fibrosis of the liver. The
capillaries passing through the liver have fenestrae
or gaps allowing the passage of much larger
molecules than most blood vessels. When blood
pressure increases in the liver though, these close
and become less permeable. Blood sinusoids serve to
dissipate the pressure of blood entering the liver
and store blood; the system is usually maintained at
low pressure. Certain bile salts can increase blood
flow and pressure within the liver.
Hepatocytes are
arranged in cords with one side abutting a blood
vessel and the other a bile canaliculus. On both
sides surface area is magnified by the presence of
microvilli, greatly increasing the surface for
nutrient, metabolite, drug, toxin and bile exchange.
These cords are supported on a framework of collagen
and reticulin fibers.
Bile is formed in
the hepatocytes and passes into the canaliculi, then
to ductules, ducts and ultimately the gallbladder.
Electrolyte and fluid content is modified during
this passage. In the gall-bladder it is concentrated
and stored until it is expelled into the duodenum to
aid in digestion.
Nutrient rich
blood from the stomach, intestines, spleen,
pancreas, colon and gall-bladder flows into the
portal circulation and passes through the liver
before entering the rest of the circulation.
Nutrients are removed and further processed while
undesirable substances absorbed from the gut are
removed and/or detoxified. At any one time 10-25% of
the blood is in the liver. Much of it is being
stored. The liver can actually double its blood
storage which alone can lead to liver congestion.
During hemorrhage, it can compensate for loss of 25%
of the total blood volume. At rest about 25% of
cardiac output is passing through the liver, this
changes with exercise, posture and at meal times.
While two-thirds of the blood in the liver comes
from the portal vein, one third comes through the
hepatic artery, which supplies the oxygen needed for
liver function. Even brief interruption of blood
flow through the hepatic artery can lead to lethal,
septic necrosis.
In newborn
puppies most of the abdominal cavity is occupied by
the liver, in the young dog the ratio of liver to
body weight is about 4 to 5: 100, but in older dogs
this drops to 2:100. Small livers may be the result
of reduced blood perfusion, chronic fibrosis,
atrophy of the hepatocytes, or loss of their
cellular content. Enlarged liver can result from
passive congestion, infiltrative or inflammatory
conditions, blockage of the bile ducts and cystic
liver disease. Drug exposure – barbiturates etc.;
infection or inflammation of the hepatocytes can
result in increased liver mass secondary to
enlargement of the organelles within the cells. If
70% of the liver is removed, in 6 weeks the
remaining liver can have regrown to pretty much
normal size and functional capacity. During that
time, the body must have adequate glucose and
coagulation factors provided, however.
Bile acids are
formed from cholesterol and bound to an amino acid,
usually taurine but sometimes glycine. Bile is
secreted in volume into the intestines when food is
consumed, and helps digestion and absorption of fat.
Bile is released in smaller quantities, sometimes
by-passing the gallbladder, at other times. Some
dogs will vomit up bile if they have not been fed –
particularly before the morning feed. Giving a
bed-time cookie is usually enough to prevent this
happening.
Early signs of
hepatobiliary disease are usually vague – anorexia,
vomiting, diarrhea/constipation, weight loss,
intermittent fever. A more specific sign would be
jaundice – yellowing of the mucous membranes and
non-pigmented skin and eye whites – this can appear
rapidly with major occlusion of the bile duct or
very slowly. Gastrointestinal ulceration and
hemorrhage may occur as disease progresses. Bleeding
tendencies, due to Vitamin K deficiency, usually
take a couple of weeks to appear. Feces may become
dark green or dark-green/orange due to increased
blood break down or pale gray or tan and fatty if
bile flow is obstructed. Significant bleeding into
the bowel produces black tarry feces. Increased
drinking and urination and the appearance of
urobilinogen in urine indicate liver disease,
although some animals have problems urinating.
Change in liver size can often be palpated.
Neurobehavioral changes – ataxia, lethargy, stupor,
head-pressing, obsessive circling, sudden
unexplained blindness, seizures or coma can indicate
severe acquired liver insufficiency or congenital
portosystemic shunt – where some or all blood from
the digestive tract by-passes the liver and goes
directly into the main circulation. Ascites, the
accumulation of fluid in the abdomen, is often the
result of increased blood pressure in the portal
vein usually indicating obstruction.
Diagnosis of
liver disease begins with basic blood testing a
complete blood count and biochemistry profile, in
fact in many cases liver disease can be discovered
before any physical signs become apparent. However,
liver enzymes can be elevated by a number of
unrelated conditions – bone disorders or growth;
endocrine disease; gastrointestinal and splenic
disease; hypoxia; drugs; low blood pressure;
neoplasia; systemic infection; trauma; fever; wasp
stings or after general anesthesia! If none of these
are apparent follow up with ultrasound and biopsy
are probably the most helpful procedures for
characterizing the cause of the liver disease.
X-rays and nuclear scintigraphy may also be helpful.
Acute
hepatic failure occurs
when a sudden severe insult to the liver results in
compromise of at least 70 to 80% of functional liver
mass, exceeding the liver’s functional reserve and
resulting in signs of liver failure. Diffuse
necrosis of liver tissue is the most obvious and
consistent sign. Causes can include hepatotoxic
drugs and anesthetic agents; chemical and biologic
substances (aflatoxin; amanita mushrooms; blue green
algae; pennyroyal oil; heavy metals; herbicides;
fungicides; rodenticides; household cleaners;
industrial chemicals, etc.); infectious or parasitic
agents (viral hepatitis, acute bacterial
cholangiohepatitis; leptospirosis; liver abscess;
extrahepatic infections and sepsis; systemic fungal
infection – esp histoplasmosis; toxoplasmosis;
postcaval heartworm infection); systemic or
metabolic disease (acute pancreatitis; acute
hemolytic anemia); trauma; diaphragmatic hernia with
liver entrapment; heat stroke; surgery where blood
pressure and oxygen perfusion is compromised; liver
lobe torsion. Treatment depends on the underlying
cause of the liver failure. Given the liver’s role
it is especially vulnerable to a vast array of
substances, and this is something we should consider
before introducing any substance into our dog’s or
our family’s environment. Apart from acetaminophen
antidotes exist for most acute hepatotoxins.
Cholestatic hepatobiliary disease is
the result of impaired flow or excretion of normal
volumes of bile. Substances normally secreted in the
bile build up in circulating blood serum – bile
acids, bilirubin, cholesterol – and there is
increased activity of enzymes associated with the
cells of the biliary tract – alkaline phosphatase
(ALP) and gamma-glutamyltransferase (GGT). Jaundice
is the hallmark of this condition. Cholestasis can
result from blockage or rupture of the bile ducts.
This often requires surgical correction. Common
causes are pancreatic disease (edema, abscesses,
cysts or cancer), or gallstones. Retention of bile
in the liver can cause secondary injury to
hepatocytes.
Chronic liver disease –
hepatic fibrosis and cirrhosis –
can also result from a great many causes. Repeated
exposure to drugs or toxins; infection; cholestasis;
immune injury (chronic idiopathic hepatitis) and
hypoxia often secondary to cardiac failure are all
potential problems. A single episode of massive
hepatic necrosis could cause end stage liver
disease. However, the cause is never determined in
most cases. One study showed that cirrhosis was
responsible for 15% of the cases of liver disease as
determined by biopsy.
In cirrhosis
fibrous tissue replaces much of the normal liver and
the remaining cells become disorganized further
limiting function. It is irreversible, and while
removing the underlying cause may slow progression
of the disease it can not restore the liver. Blood
flow to the liver is compromised, and blood pressure
increased, so remaining cells are less able to
function.
Nodular
hyperplasia is
a common post-mortem finding in dogs over the age of
8. These nodules are not precursors to cancerous
lesions, and they are not associated with clinical
signs. Unfortunately, they cannot be distinguished
from primary or secondary neoplasia on ultrasound,
only by biopsy.
Liver
cancer may
be primary or metastatic and virtually all types of
cancer have been reported. Metastatic cancer from
pancreas, lymph nodes, spleen, mammary glands,
adrenal glands, bone, bone marrow, lungs, thyroid
glands and gastrointestinal tract is more common,
and lymphosarcoma and pancreatic carcinoma are the
most common types. Primary tumors are rare, and they
are not associated with viral infection, exposure to
chemical carcinogens, toxins, drugs or prior liver
disease as they are in humans. These tumors can be
benign or malignant.
I am not aware of
any cases of congenital portosystemic shunts being
reported in Beardies. Multiple acquired
portosystemic shunts can result as a compensatory
response to prolonged elevated portal blood
pressure. Likewise hepatic arteriovenous fistulas
can form as a result of elevated blood pressure in
the hepatic artery diverting blood into the portal
system. Neither condition is common. Both are more
common in younger dogs, and in certain breeds, but
not in beardies.
Hepatic
lipidosis is
an excessive accumulation of fat (triglycerides) in
the liver. It is caused by an imbalance between rate
of deposition and dispersal of fat, and can be
nutritional, metabolic, hormonal, toxic or hypoxic
in origin. The clinical significance depends on the
severity and underlying cause. Excess fat does not
impair liver function, but results in a large, pale
yellow liver – such as that of the foie gras goose.
Diabetes mellitus is one of the most common causes.
Treating the underlying cause is desirable.
Hypertriglyceridemia –
elevated triglyceride (TG) levels in serum - is the
most prevalent lipid disorder in dogs. It may result
in vomiting, diarrhea and non-localized abdominal
pain. Signs frequently resolve with fasting.
Seizures may also be a presenting sign. Reducing
dietary fat is often curative, but feeding
gastrointestinal diets (such as Hill’s i/d) may make
the condition worse. Blood triglycerides must be
measured after fasting the dog to distinguish the
condition from normal post feeding elevation of TG.
Other rule-outs include diabetes mellitus, which can
result in marked increase in TG and mild elevation
of cholesterol (CH); protein losing nephropathy due
to kidney disease which increases both TG and CH.
The primary cause of elevated CH is hypothyroidism,
although 30% of dogs with Cushing’s Disease (hyperadrenocorticism)
have elevated CH, too.
The major
function of the exocrine
pancreas is
to secrete digestive enzymes and coenzymes. It also
secretes bicarbonate to help neutralize stomach
acid, and factors that assist in absorption of
Vitamin B 12, zinc and probably other nutrients.
Pancreatic fluid inhibits bacterial overgrowth in
the duodenum and jejunum, helps with normal
degradation of old brush border cells, and promotes
growth of the mucosa together with biliary
secretions. The pancreas protects itself from
digestion by several mechanisms, including producing
an enzyme inhibitor (pancreatic secretory trypsin
inhibitor), which it secretes together with the
digestive enzymes.
The pancreas has
left and right lobes and a small central body where
they join together. Embryonically it grows out from
the duodenum to which it stays connected by two
secretory ducts –pancreatic duct and accessory
pancreatic duct. The right lobe lies alongside the
duodenum and the left lobe along the pyloric region
of the stomach.
The acinar cells
of the pancreas secrete enzymes to degrade proteins,
lipids and polysaccharides. Proteolytic and
phospholipolytic enzymes are stored as inactive
zymogens, which are normally activated in the
intestines by cleaving a small peptide from the
zymogen, so trypsinogens become trypsins etc. This
is achieved by an enzyme – enteropeptidase – formed
in the enterocytes. The trypsins, chymotrypsins and
elastases cleave polypeptides at specific sites,
while carboxypeptidases lop off terminal carboxyl
residues.
At rest the
pancreas secretes about 2% of the bicarbonate and
10% of the enzymes it does when the animal eats a
meal. There are cyclic increases though in the
amounts secreted. After a meal secretion occurs in
two phases, the first, which peaks an hour or two
after eating, is rich in enzymes. The second phase
occurs about 8 to 11 hours after the meal, is more
voluminous and rich in bicarbonate. Low levels of
amylase, lipase and zymogens leak into the blood
stream.
Pancreatitis is
inflammation of the exocrine pancreas. Acute
pancreatitis has a sudden onset, may occur
repeatedly, but causes little or no permanent
pathologic change. Chronic pancreatitis is a
continuing inflammatory condition resulting in
permanent impairment of function. Pancreatitis seems
to result when the proteolytic enzymes are activated
while still in the pancreas causing autodigestion.
This is probably because of a failure of the normal
secretory process. In most cases the inciting cause
is unknown. Some potential causes are:
nutrition/hyperlipoproteinemia – low protein, high
fat diets, and especially prevalent in obese
animals; drugs, toxins, hypercalcemia; duct
obstruction – gall stones, tumors, parasites,
trauma, edema, sphincter spasm; duodenal reflux,
pancreatic trauma, loss of circulation/reperfusion
injury; viral, fungal or parasitic infection.
Signs usually
include depression, anorexia, vomiting, sometimes
diarrhea and pain – splinting the stomach (praying).
In severe cases the dog may have collapsed and be in
shock. They are usually mildly to moderately
dehydrated and have a fever. In some dogs a mass at
the front of the abdomen can be felt. CT scans are
the most useful for diagnosing pancreatitis, but
ultrasound may be helpful. Fluids and careful
electrolyte balance together with nothing given by
mouth is the basis for treatment. In uncomplicated
cases, prognosis is good for complete recovery,
although it is recommended that high fat foods be
avoided in future.
Exocrine
pancreatic insufficiency (EPI) is
quite common in Beardies. Pancreatic acinar cells
are progressively lost and replaced by fibrous
tissue so that the body ultimately fails to produce
sufficient digestive enzymes and food is not
absorbed but passes through to the feces largely
unchanged. Signs do not appear until most of the
tissue is lost, for example fat in the feces is
usually not observed until 85-90% of the secretory
capacity has been lost. Even without pancreatic
enzymes, alternate pathways do exist, and up to 63%
of ingested protein and 84% ingested fat will be
absorbed without pancreatic enzymes.
In the majority
of dogs pancreatic acinar atrophy is the primary
cause of EPI. The cause is unknown, although
nutritional deficiencies – amino acid imbalance,
copper deficiency, protein-calorie malnutrition –
have been postulated. Malnourishment secondary to
small intestinal mucosal abnormality has also been
suggested as dogs often show g/I disturbance long
before there is significant weight loss. In humans,
and apparently in quite a lot of Beardies, chronic
pancreatitis is the cause of EPI. In some cases
diabetes mellitus may co-exist with EPI. In some
dogs congenital EPI has been reported, as well as
EPI secondary to surgical resection of the duodenum.
In many dogs with
EPI, enzymes malfunction, there are changes in the
mucosa of the small intestine resulting in
abnormalities of transport mechanisms and changes in
bacterial presence. Dogs have often suffered from
malabsorption a long time before diagnosis is made
or help sought however, and this may result in some
of the associated changes that have been reported.
The best test for
EPI is a blood test – serum trypsin-like
immunoreactivity (TLI). This test rules out small
intestinal disease (IBD) as the cause of the
malnourishment. Dogs are managed by supplementing
each meal with pancreatic enzymes and most do quite
well. The enzymes – especially lipase – are largely
digested themselves though before they reach the
small intestine. Attempts to maximize enzyme
efficacy - such as predigesting food with enzymes
prior to feeding - have not proven to have any
advantage. Highly digestible diets should be fed,
and in most cases dogs require slightly more food
than their healthy counterparts to maintain their
ideal weight. Like all exocrine pancreatic diseases,
EPI can be very painful and dogs may become more
aggressive as a result of the pain as well as
hunger. Vitamins B 12 and E may need to be
supplemented in dogs with EPI.
Adenocarcinoma of
the acinar or pancreatic duct cells is relatively
uncommon in dogs. When it does occur, the dogs are
older. These tumors are highly malignant and have
usually metastasized to the duodenal wall, liver and
lymph nodes prior to diagnosis. Signs are usually
non-specific - anorexia, depression, vomiting. If
the bile ducts are involved the dog may develop
jaundice, if the pancreatic duct is blocked there
will be signs of EPI, and if the beta cells are
affected signs will be of diabetes mellitus. An
abdominal mass may be palpated, or a tumor
visualized via ultrasound, but diagnosis is usually
made via exploratory surgery. Prognosis is extremely
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