Most common cause development of exocrine pancreatic insufficiency (EPI) in dogs is atrophy of the secretory acini in the pancreas. Most often this pathology detected in German Shepherds, however, the disease can develop in dogs of other breeds, including mixed breeds. German Shepherds are known to have a genetic predisposition to NEFP, but the etiology of this phenomenon is unknown. The disease is progressive: at a young age, the exocrine function of the pancreas is normal; the first clinical signs of the disease begin to appear in animals aged 1 to 5 years. In other cases, NEFP may be caused by chronic, recurrent inflammation (pancreatitis), as commonly seen in cats, and pancreatic hypoplasia. NEFPZh and diabetes often complicate the course of chronic pancreatitis in dogs.

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2.1 Pathophysiology

Clinical signs of NEFP usually appear when the secretory activity of this organ is reduced by approximately 90%. Insufficiency of digestive enzymes leads to disruption of the processes of digestion and absorption in the intestines. In addition, abnormal activity of digestive enzymes in small intestine, traffic violation nutrients, atrophy of intestinal villi, infiltration of intestinal mucosa with inflammatory mediator cells were established in all cases of NEFP. A common complication accompanying the disease is a violation of the intestinal microflora, which often leads to enteropathies caused by taking antibiotics (EPA).TABLE OF CONTENTS

2.2 Clinical symptoms and results of general physical examination

The three classic signs of NEFP are chronic unexplained diarrhea, weight loss, and polyphagia. In this case, feces are poorly formed and are excreted in large quantities and have signs of steatorrhea. Often observed loose stool. Sick animals often have a tendency to coprophagia, and vomiting is rare. Dog owners celebrate their pets severe flatulence and rumbling in the stomach. Externally, dogs with NEFP appear emaciated, muscle mass their hair is reduced, their coat loses its shine and becomes unpleasant and greasy to the touch. However, animals are physically active and mobile. If your dog is lethargic, refuses food, and has a fever, another medical condition is likely causing the diarrhea.TABLE OF CONTENTS

2.3Diagnostics

Many laboratory tests are used to diagnose NEFP, with the most effective method- definition trypsin-like immunoreactivity (TPIR) in the blood. Kits for determining TPIR are strictly species-specific, so only special kits should be used for dogs and cats (for example, a kit is used for catsfTLI from GI-Lab , USA). Other laboratory research(biochemical or hematological) do not give a specific result, but they are necessary to identify concomitant diseases. If helminth infestation or bacterial contamination is suspected, feces are examined (for the presence of helminth eggs and for bacteriological cultivation).

TPIR measures the amount of trypsinogen in the patient's blood. The only source trypsinogen in the body is the pancreas, so the test result indirectly reflects the amount of functionally active glandular tissue. The determination of TPIR is carried out after a 12-hour fast and is very sensitive and specific. Values below 2.5 µg/l clearly indicate NEFP, while values in the range of 2.5-5 µg/l correspond to the norm. TPIR is stable at room temperature and can remain unchanged for several days, but it quickly degrades when heated. Therefore, samples, especially in summer, should be protected from direct sunlight. If the content of TPIR in the patient’s blood is normal, the diagnosis of NEFP is excluded.TABLE OF CONTENTS

2.4 Treatment

Most dogs and cats with NEFP have a good clinical response to enzyme replacement therapy .Convenient In general, use powdered enzyme substitutes without special coatings. The initial dosage is 2 teaspoons of powder for every 20 kg of animal body weight with each portion of food. It must be emphasized that enzyme substitutes must enter the animal’s body with every portion of food, even with treats. Otherwise, diarrhea may return. Enzyme replacement tablets or capsules for cats and dogs are less effective than powders. The clinical symptoms of NEFP are weakened after the start of enzyme replacement therapy, and in the future the dose of enzyme replacement can be gradually reduced until the minimum effective dosage is identified. It should be kept in mind that different batches of replacement enzymes may have different enzymatic activities. Enzyme replacement therapy should not be added to the treatment of NEFP. pre-treatment feed with enzyme preparations for 30 minutes, administer drugs that reduce the acidity of gastric juice (for example, type 2 histamine receptor antagonists) and enrich the animal’s feed with salts bile acids or soda. Very good substitutes for pancreatic enzymes are fresh frozen pig pancreas. When stored frozen at -20°C, they retain a large amount of active enzymes for 1 year.

Enzyme replacement therapy is a good addition to cats with NEFP. parenteral administration cobalamin, since with this pathology the absorption of vitamin B 12 in the digestive tract is impaired.TABLE OF CONTENTS

3Pancreatitis

Pancreatitis in cats and dogs is difficult to diagnose, but careful examination can reveal a number of symptoms. The easiest way to identify is acute necrotizing pancreatitis, the outcome of which is usually unfavorable. Sluggish, recurrent acute or chronic pancreatitis is most common in cats and quite common in dogs. Treating pancreatitis is quite difficult. Severe acute forms require immediate hospitalization of the patient and intensive care to prevent death. At the same time, sluggish chronic pancreatitis can be treated at home with the help of appropriate diet therapy.TABLE OF CONTENTS

3.1.Definitions and pathophysiology

Pancreatitis in small domestic animals represents a variety of forms of diseases that vary in severity - from mild subclinical forms that occur without obvious symptoms to acute necrotizing pancreatitis, which most often ends in the death of the patient. The classification of forms of pancreatitis is based on histopathological changes in the tissues of the pancreas:

Acute pancreatitis: neutrophil infiltration, necrosis, edema. The changes are potentially reversible.

Chronic pancreatitis: monocyte infiltration, fibrosis. Usually has a relapsing course.

These types of disease, in turn, are divided into subtypes, including acute necrotizing pancreatitis (in which there is severe necrosis of the fatty tissue surrounding the pancreas) and active chronic pancreatitis (characterized by infiltration of the pancreatic tissue with both neutrophils and monocytes against a background of nodular pancreatic hyperplasia and fibrosis) . Histopathological classification is useful for understanding the mechanisms of disease development, but is not very useful clinically. In this regard, it is more convenient to use a classification based on the characteristics of the clinical course of the pathology, taking into account scores for the severity of pancreatitis and its symptoms (see table).

Scoring system for assessing the severity of pancreatitis in dogs and cats (according to Ruaux , 2000)

Severity	Score*	Forecast	Typical Therapy Techniques
Lightweight		Good	Self-healing often occurs. In the absence of signs of dehydration, therapy can be carried out at home. If necessary, intravenous fluid therapy. Treatment using the method of “unloading” the pancreas + (if necessary) analgesic therapy.
Average		Good to favorable	There are usually signs of dehydration due to prerenal renal failure. Treatment: solutions of crystalloids (2 maintenance doses) and electrolytes. No drugs per osuntil the vomiting stops! Pain therapy. With properly selected fluid therapy full recovery, without complications and consequences. If the animal is starving for more than 2 days, additional nutritional support is necessary.
Average		From good to bad	Dehydration and hypovolemia are observed due to prerenal renal failure. Degenerative shift to the left in leukocyte formula. Intensive therapy is required. Shown intravenous administration solutions of crystalloids at a speed that provides anti-shock effect, then the introduction of solutions of blood-substituting colloids. In many cases, transfusion of donor blood plasma is indicated. Urinary output, renal and pulmonary function should be monitored. Use of analgesics and special nutritional support. It is necessary to monitor the condition of the blood coagulation system and, if necessary, administer donor plasma and heparin. In case of insufficient efficiency therapeutic activities hospitalization is indicated.
Heavy		Bad	Intensive therapy And resuscitation measures+ constant observation + immediate hospitalization.
Heavy		Very bad	Immediate care may be required surgical intervention and conducting peritoneal lava-zha. Application shown artificial respiration. Liquid therapy in large volumes. The nutrition is completely parenteral. Most patients die.

*Note: The scoring system for assessing the severity of pancreatitis is based on the number of organ systems involved. pathological process and damaged as a result of illness at the time of application for veterinary care.

The pathophysiology of pancreatitis is still not fully understood. Acinous cells of a healthy pancreas secrete enzymes involved in the initial stage of digestion of food components (the products of their activity, relatively low molecular weight compounds, are further destroyed by enzymes of the brush border of the cells of the small intestinal mucosa). Pancreatic enzymes include lipase (the pancreas is the main source of this enzyme), a-amylase, phospholipase, proteolytic enzymes (elastase, chymotrypsin and trypsin). Normally, pancreatic cells are protected from the effects of produced enzymes due to the fact that many of them are synthesized in the form of inactive precursors, so-called zymogens (for example, trypsinogen and chymotrypsinogen). Zymogens accumulate in special granules separated from lysosomes. In addition, the contents of the granules contain a pancreatic trypsin inhibitor, which prevents the premature activation of this enzyme. Trypsin activation occurs in the lumen of the small intestine under the action of enterokinase. The activated trypsin then activates chymotrypsin.

The main link in the pathogenesis of pancreatitis is the unacceptable fusion of lysosomes with granules containing zymogens in acinar cells of the pancreas. The acidic environment of lysosomes inactivates secreted trypsin and other enzymes in cells, causing local " self-digestion", is developing inflammatory reaction and necrosis of the acini of the pancreas, and then necrosis of the fatty tissue surrounding the pancreas. Free enzymes enter the abdominal cavity, where they cause local or extensive peritonitis, as well as into the bloodstream. In the blood, pancreatic enzymes are relatively quickly inactivated by a number of plasma protease inhibitors, in particular, α-1-antitrypsin (also known as plasma protease inhibitors). a r protease inhibitor"). Inhibitor o ^- antitrypsin temporarily binds proteases and then transfers them to a 2 -macroglobulin, which, in turn, binds these enzymes irreversibly. The resulting complex of pancreatic enzyme and o ^- macroglobulin excreted by the reticuloendothelial system. For severe pancreatitis, the number of proteinase inhibitors V blood decreases, and free active proteolytic enzymes appear in the plasma. The action of these enzymes, as well as the activation of neutrophils and monocytes, the absorption of endotoxins from the lumen of the gastrointestinal tract into the bloodstream and the release pro-inflammatory cytokines and reactive oxygen radicals directly from the tissues of the pancreas and leukocytes into the blood, alveoli and other organs lead to generalized inflammatory reaction, vasodilation, increased blood clotting and simultaneous activation of fibrinolysis. In particular severe cases Disseminated intravascular coagulation (DIC) may occur. The functions of many organs are impaired, especially the kidneys (prerenal and/or renal azotemia develops) and lungs (in especially severe cases, pulmonary edema and acute respiratory failure may develop).

The factors leading to the development of pancreatitis in each specific case are not fully known. Under experimental conditions, it is possible to induce the development of pancreatitis by obstructing the secretory duct of the gland. In this case, the disease is usually mild, although it can be aggravated by stimulating the secretory activity of the pancreas. Obstruction of the excretory duct caused by a neoplasm in the pancreas due to cholangitis or inflammation of the intestine can cause pancreatitis. This is especially true for cats that have the excretory duct of the pancreas at the confluence with the duodenum merges with the bile duct.

In dogs, the development of pancreatitis is often preceded by overeating fatty foods. It is possible that in in this case The pathogenetic mechanisms leading to pancreatitis begin with gastric overfilling and stimulation of increased secretion in the pancreas. An important factor contributing to the development of pancreatitis is hypertriglyceridemia(hereditary or caused by diet or endocrine disorders). Pancreatitis can also result from taking certain medications. However, regarding steroids, the data are contradictory: these drugs actually increase the activity of lipase in the secretion of the gland by 5 times, but so far in the experiment they have not been able to induce pancreatitis.TABLE OF CONTENTS

3.2 Clinical symptoms

Clinical signs of pancreatitis vary depending on the severity of the disease. The classic triad of symptoms (vomiting + severe cranial abdominal pain ± “praying position”) in dogs and cats is observed only in severe, acute cases. Pancreatitis is often accompanied by acute colitis, in which fresh blood is observed in small amounts of feces - this is a consequence of local peritonitis spreading to the transverse colon, adjacent to the left lobe of the pancreas. In severe cases, the patient experiences collapse and signs of dehydration against the background of shock symptoms, and in especially severe cases, acute renal failure, respiratory failure, and disseminated intravascular coagulation syndrome.

In other, milder forms of acute or chronic pancreatitis, the symptoms of the disease may be mild. Usually it is represented by anorexia with or without mild attacks of colitis, periodic vomiting, increased flatulence and mild abdominal pain. These forms of pancreatitis are especially common in cats. In these animals it is often very difficult to distinguish pancreatitis from cholangitis or intestinal inflammation. In addition, in cats, these pathologies often accompany each other, which further complicates diagnosis.

With pancreatitis, there is a risk of developing acute or chronic complications. Acute forms diseases can cause dehydration, acidosis, electrolyte imbalance as a result of transient vomiting and anorexia (hypokalemia, hypochloridemia, hyponatremia), prerenal azotemia, and in some cases, a systemic inflammatory response, hypotension, respiratory failure and disseminated intravascular coagulation syndrome. In cats, acute pancreatitis is often accompanied by the development of hepatic lipidosis. Pancreatitis in cats (less often in dogs) is also accompanied by cholangitis and cholangiohepatitis, which is determined by the anatomical proximity of the proximal pancreas and bile duct in both species. The liver tissue is affected due to inflammatory mediators entering it with blood from the portal vein.

Chronic pancreatitis can cause the destruction of so much of the secretory units of the pancreas that the patient develops diabetes mellitus, NEFP, or both diseases simultaneously. In people with chronic pancreatitis, diabetes mellitus usually develops earlier, which precedes the development of NEFP by several months. This is due to the fact that diabetes mellitus begins to manifest clinically with the loss of 80% of the active glandular tissue of the pancreas, and NEFP - with the loss of 90% of this tissue.TABLE OF CONTENTS

3.3 Laboratory diagnostics

Diagnosing pancreatitis is quite difficult because modern stage There are no specific and sensitive diagnostic methods other than histopathological examination of pancreatic tissue biopsies obtained during surgery, laparoscopy or postmortem. Clinical symptoms and medical history suggest the presence of pancreatitis, especially when acute course: If your dog is constantly vomiting and has severe pain in the front of the abdomen after overeating, there is reason to suspect acute pancreatitis. However, such symptom complex may also be a consequence of partial or complete intestinal obstruction, volvulus, intussusception or perforation of a stomach ulcer. With a milder course of pancreatitis in both cats and dogs clinical symptoms become nonspecific: similar signs are observed when various diseases gastrointestinal tract, liver, etc. For differential diagnosis further research is needed.

In the absence of biopsies, diagnosis of pancreatitis is usually based on clinicopathological tests and ultrasound examination of the pancreas. At clinical analysis blood most often reveals neutrophilic leukocytosis with a shift of the formula to the left (with severe forms- with a degenerative shift to the left). As the patient dehydrates, the hematocrit increases. Chronic pancreatitis in cats in 20-80% of cases is accompanied by mild anemia, which is rarely observed in dogs. In severe cases, the platelet count decreases due to DIC. Hypokalemia is common in both dogs and cats. It is often accompanied by hyperglycemia (glucose can even be detected in the urine) due to stress and the release of hydrocortisol, catecholamines and glucagon into the blood. But cats with suppurative pancreatitis may experience hypoglycemia. Although one of the possible causes of pancreatitis is considered hypercalcemia, the course of the disease leads to the development of mild hypocalcemia and hypomagnesemia due to saponification of fats in the adipose tissue surrounding the pancreas. With pancreatitis, very often detected hypercholesterolemia And hypertriglyceridemia in blood samples obtained during fasting. These deviations can be both a cause and a consequence of pathological processes in the pancreas. In severe acute cases, azotemia associated with prerenal renal failure and kidney damage due to dehydration and toxins. To clarify the severity of kidney damage, it is useful to determine the specific gravity of urine and examine its sediment. In the blood of patients with pancreatitis, due to damage to liver cells by toxins entering this organ through the portal vein, the activity of liver enzymes is often slightly or moderately increased.

The above changes are nonspecific. Monitoring these indicators is useful for assessing the effectiveness of therapy for pancreatitis, but not for diagnostic purposes. To diagnose the disease, the activity of pancreatic enzymes: amylase, lipase and trypsin is determined in the patient’s blood. For amylase and lipase, a direct catalytic determination is carried out, estimating the number of active centers, and for trypsin, a determination trypsin-like immunoreactivity (TPIR). Sometimes the content of specific pancreatic lipase (SPL) is also analyzed. This enzyme is determined immunologically by antigens that are not part of its active center. Immunological methods are convenient in that they allow identifying not only the active forms of enzymes, but also the corresponding zymogens. All immunological tests are strictly species specific.

In dogs, determining the level of pancreatic enzymes in the blood is the main method for diagnosing the disease. These tests are not always sufficiently sensitive and specific, but they are the most accessible and common. It would be ideal to supplement the obtained data with ultrasound examination of the pancreas. The content of pancreatic enzymes in the blood of dogs that corresponds to the norm does not exclude the presence of pancreatitis! The level of amylase rarely increases in comparison with the level of lipase and TPIR in pancreatitis, therefore, during a diagnostic study, it is not enough to determine the level of amylase in the blood only. When diagnosing the disease, the level of all three pancreatic enzymes in the patient’s blood should be determined.

In cats, there are no methods for determining the levels of amylase and lipase in the blood. diagnostic value. The TPIR test is the only test available to diagnose pancreatitis in cats. The specificity of the TPIR test for pancreatitis in cats is about 80%, and the sensitivity of the test is 46-80%. This is much higher than other diagnostic methods that do not involve obtaining pancreatic tissue samples.

It is optimal, however, to supplement the determination of TPIR in cats with ultrasound examination of the pancreas. Ultrasound diagnostics are good at identifying acute necrotizing forms of pancreatitis, in which enzyme production is weakened, and the determination of TPIR is especially convenient for diagnosing chronic pancreatitis, when changes in the pancreas are not noticeable during ultrasound examination.

Other diagnostic techniques are currently used in humans, dogs and cats only to clarify the diagnosis and predict the outcome of pancreatitis. They include definition trypsin-activating peptide (TPA) in urine and blood serum, the content of trypsin complex in the bloodά 1 -inhibitor proteinase and pancreatic lipase immunoreactivity (PLI) in dogs. In medicine, the content of the series is also determined pro-inflammatory cytokines in the blood serum, which makes it possible to clarify the prognosis of the outcome of the disease.TABLE OF CONTENTS

3.4 Instrumental diagnostics

Along with determining the content of pancreatic enzymes in the patient’s blood ultrasonography Ultrasound of the pancreas is one of the few specific methods for diagnosing pancreatitis. However, the location of the pancreas in dogs and cats places increased demands on the qualifications and experience of the specialist conducting the examination. Ultrasound makes it possible to diagnose pancreatitis because this pathology is accompanied by edema of the gland, its swelling, necrosis of the adipose tissue surrounding the gland, and peritonitis. Using ultrasound, you can also identify neoplasms, abscesses or pseudocysts in the pancreas, as well as diagnose cholangitis and thickening of the walls of the small intestine near the gland.

Radiography abdominal cavity It only allows you to clarify the diagnosis of pancreatitis. It can be used to identify whether a patient has foreign bodies V gastrointestinal tract, which can be important for differential diagnosis. For acute pancreatitis in cats and dogs radiographically a decrease in density and local peritonitis in the anterior abdominal cavity is detected. The ventrodorsal projection reveals dilatation of the duodenum and its displacement lateral and dorsal to the normal position, caused by swelling of the pancreas. The transverse colon also moves, most often in a caudal direction. Contrasting It is better not to use barium: it does not provide significant advantages, and filling the lumen of the gastrointestinal tract with a contrast agent stimulates the secretion of pancreatic enzymes in the affected pancreas.. TABLE OF CONTENTS

3.5 Treatment

The method of treating pancreatitis in dogs and cats is largely determined by its form and severity at the time of seeking veterinary help. If the cause of pancreatitis can be identified (for example, hypercalcemia), it should be eliminated. In most cases, pancreatitis is idiopathic character, and only symptomatic therapy is possible. In addition, it is necessary to identify and treat concomitant pathologies that complicate the course of the disease (cholangitis, intestinal inflammation, in cats - liver lipidosis).

With severe necrotizing pancreatitis (3-4 points) in cats and dogs, the prognosis for the outcome of the disease is very unfavorable. Typically, such patients are severely impaired water-electrolyte balance against the background of a systemic inflammatory reaction, there is renal failure and increased risk DIC syndrome. Patients are indicated for intensive therapy, including blood plasma transfusions and tube feeding (in some cases, a complete transfer to parenteral nutrition). It is best to hospitalize the patient in a specialized veterinary clinic. The prognosis for the outcome of the disease is very unfavorable.

Mild forms of pancreatitis (score 0) may require hospitalization for 12-24 hours for intravenous fluid therapy, especially if the patient is vomiting and there are signs of dehydration. If there are no signs of dehydration, and general state the animal is satisfactory, it can be treated at home using the method of “unloading” the pancreas (enteral administration of fluids) for 24-48 hours. If necessary, the animal is given analgesics. For a long time, the animal is fed an appropriate diet. In animals with chronic pancreatitis Mild gastrointestinal symptoms and anorexia are usually observed periodically.

Moderate forms of pancreatitis (1-2 points), accompanied by vomiting and dehydration, require hospitalization, during which patients undergo fluid therapy, fasting treatment and pain relief. In many cases, the use of antibiotics is indicated, and in some cases, blood plasma transfusion is indicated. .TABLE OF CONTENTS

3.5.1 Intravenous administration of fluids and electrolytes

Intravenous fluid therapy is important for any form of pancreatitis, but is especially effective for milder forms of the disease. It eliminates fluid and electrolyte imbalance caused by vomiting and ensures sufficient blood flow through the pancreas. Fluid therapy uses solutions of blood substitutes (in particular, lactated Ringer's solution). The rate of administration and the volume of fluid infused depend on the degree of dehydration of the patient. For pancreatitis of mild or moderate severity (0-1 points), a maintenance rate of fluid administration is usually sufficient. in more severe forms of the disease, it is necessary to combat developing shock (infusion rate up to 90 ml/kg/hour for 30-60 minutes). In such cases, after therapy with Ringer's solution, it is necessary to administer solutions of synthetic colloids. The content of electrolytes in the patient's blood should be closely monitored Severe pancreatitis is usually accompanied by hyponatremia, hypochloremia, hypocalcemia and hypomagnesemia, while hypokalemia is particularly dangerous and requires immediate correction. Blood potassium levels should be measured and additional amounts given as needed potassium chloride into the infused liquid. Intravenous fluid therapy in the setting of fasting and increased renal potassium loss may worsen hypokalemia by increasing renal excretion and decreasing absorption. Given this phenomenon, it is recommended to increase the amount of potassium in lactated Ringer's solution from the usual 5 mEq/L to 20 mEq/L. The rate of introduction of potassium into the body, as a rule, should not exceed 0.5 mEq/l/kg/hour.

In especially severe cases (2-4 points), blood plasma transfusion is recommended. This allows you to replenish your reserves o^ - A ntitrypsin and (x2-macroglobulin in the patient’s blood. Blood clotting factors are introduced with donor plasma, therefore, to reduce the risk of DIC, it is better to supplement plasma transfusion with heparin.TABLE OF CONTENTS

3.5.2 "Unloading" of the pancreas

“Unloading” of the pancreas occurs during complete fasting and is traditionally used in the treatment of acute pancreatitis. When “unloading”, stimulation of the pancreas caused by filling the stomach or the entry of proteins and fats into the lumen of the duodenum is minimized. However this technique excluded for the treatment of people and animals with signs of malnutrition and exhaustion. In addition, even with a normal animal weight, this approach is not always acceptable - in cats, for example, anorexia Painkillers and anti-inflammatory drugs

Pancreatitis in both humans and animals is accompanied by severe pain. Patients in the clinic should be closely monitored and pain relief administered if necessary. Opiates are often used for this - morphine and its analogues (in particular, buprenorphine). Non-steroidal anti-inflammatory drugs are contraindicated for pancreatitis - their use increases the risk of ulceration in the gastrointestinal tract and potentiates the development of renal failure in animals with arterial hypertension and shock. Steroids should not be used for pancreatitis - it has not been proven that these agents reduce inflammation in the pancreas, but it is well known that steroids reduce the activity of the reticuloendothelial system. .TABLE OF CONTENTS

3.5.4 Antibiotics

For pancreatitis infectious complications They are relatively rare, but if they occur, they are very severe. In these cases, the use of antibiotics significantly reduces mortality. Therefore, broad-spectrum antibiotics are recommended for patients with acute pancreatitis, since it is not always possible to assess the risk of sepsis. For antibiotic therapy enrofloxacin and trimethoprim sulfate, which penetrate the pancreatic tissue and are effective against most pathogenic bacteria. Metronidazole is added to patients who have concomitant inflammation of the large intestine and bacterial overgrowth in the small intestine. This drug (in combination with ampicillin) is also effective for cholangitis. .TABLE OF CONTENTS

3.5.5 Antiemetics and prevention of ulceration in the gastrointestinal tract

Antiemetics help stop the uncontrollable vomiting that often occurs in patients with pancreatitis. In this case good effect(especially in dogs) gives the use of metoclopramide. However, this drug stimulates gastric motility, which in some animals increases pain and increases the production of pancreatic enzymes. In such cases, antiemetic drugs from the phenothiazine group should be used, for example, chlorpromazine. Patients with acute necrotizing pancreatitis are at increased risk of gastrointestinal ulceration due to local peritonitis. Their condition should be closely monitored, and if symptoms of an ulcer appear, sucralfate and acid inhibitors of gastric secretion should be used. .TABLE OF CONTENTS

3.5.6 Diet: initiation of feeding and dietary rations for long-term use

The composition of the diet for long-term feeding of sick animals depends on the medical history, in particular, on whether a single attack has been observed acute pancreatitis or the patient suffers from recurrent chronic pancreatitis. In the latter case, there is no other way to prevent the occurrence of exacerbations other than transferring the animal to a special diet with low content fat It is believed that in some cases, to enhance the effect, a small amount of pancreatic enzymes should be introduced into the diet. In humans, this technique reduces pain somewhat, but it is not clear how effective it is in preventing relapses of the disease. . DipECVIM- CA, MRCVS, ILTM

Reto Neiger received his degree in veterinary medicine in 1988 in Switzerland. After this, he spent a year combining work as a veterinarian and researcher, which gave him the opportunity to obtain a degree Dr th rays, etc. Occurs without prior sensitization of the body.

Excess selenium abundantia seleni (from the Latin abundantia excess - selenum selenium) is an endemic disease caused by an excess of selenium in soils and plants. Manifested by emaciation, stunted growth, hypotension of the forestomach, softening of the horns and hooves, and hair loss.

Isosthenuria , isosthenuria (from rp. isos identical + sthenos strength + uron urine) - excretion of low-density urine, reduced concentration function of the kidneys.

Icterus- cm. Jaundice.

Ileus , ileus (from the gr. eileo I twist) - mechanical intestinal obstruction. There are I. obstructive (clogging from the inside with stones, bezoars, calculi, helminths, etc.), strangulation(rotations, strangulations, invaginations

The prevalence of exocrine pancreatic disease in cats has traditionally been considered low. However, a recent retrospective study of necropsy data found that 1.3% of 6504 feline pancreatic specimens had significant pathological lesions. In contrast, of 180,648 cats entered into the Purdue University veterinary medical database over a 10-year period, only 1,027 (0.57%) had exocrine pancreatic disease. From this we can conclude that although this disease occurs quite often in cats, in most cases it is not clinically diagnosed.

Pancreatitis

Classification
In humane medicine, a fairly simple classification of pancreatitis has been created. Since there is no such classification in veterinary medicine, the authors will have to resort to the help of what is already available. So, acute pancreatitis is an inflammatory condition of the pancreas, which is completely reversible after eliminating the cause that caused it. In contrast, chronic pancreatitis is characterized by irreversible histopathological changes in the exocrine pancreatic tissue, which most often manifest as fibrosis and atrophy. Both forms of pancreatitis can be mild or severe. Weak degree disorders lead to minor tissue necrosis or necrosis does not occur, and there are no systemic signs of damage, while cases of recovery are observed quite often. Severe disorders lead to extensive necrosis of pancreatic tissue and numerous organ lesions, which often indicates a poor prognosis.

Etiology and pathogenesis
Numerous studies of experimentally induced pancreatitis in cats and other animals have led to the generally accepted hypothesis that the pancreatic acini respond uniformly to a wide variety of noxious stimuli. An initial decrease in enzyme secretion follows the formation of pathological cytoplasmic vacuoles, which contain granules of lysosomes and zymogens. This leads to inappropriate intracellular activation of trypsin, and then other digestive zymogens. Their activation provokes local consequences: inflammation, bleeding, acini necrosis and peripancreatic fat necrosis. Digestive enzymes enter the bloodstream, which can cause a variety of systemic effects, including inflammation, vasodilation leading to hypotension, pulmonary edema, disseminated intravascular coagulation, central nervous system dysfunction, respiratory failure, and multiple organ lesions.

Serious diseases and risk factors can provoke the development of pancreatitis in cats. Traumatic pancreatitis, which occurs as a result of accidents or falls from great heights, and infectious pancreatitis, which is most often caused by infestation, have also been reported. Toxoplasmagondii, and sometimes Amphimerus pseudofelineus. There is not very reliable evidence that pancreatitis can be triggered by parvovirus infection in kittens, as well as herpesvirus-1 and infectious feline peritonitis virus. There are reports of two cases caused by topical use of fenthion, an organophosphorus cholinesterase inhibitor. In addition, pancreatitis in humans and dogs is caused by many other drugs (see previous article), including azathioprine, chlorothiazide, hydrochlorothiazide, estrogens, furosemide, tetracycline, sulfonamide, L-asparaginase, 6-mercaptopurine, methyldopa, pentamidine, nitrofurantoin , didexyinosine, valproic acid and procainamide. However, there have been no reports of these substances causing pancreatitis in cats. Cats with pancreatitis may have both cholangitis and cholangiohepatitis, but there is no evidence that they are the cause of the disease. More than 90% of cases of pancreatitis in cats are idiopathic.

Clinical symptoms in cats with pancreatitis are nonspecific. In a recent study of 40 cats with severe pancreatitis, lethargy was observed in 100% of cases, anorexia in 97%, dehydration in 92%, hypothermia in 68%, vomiting in 35%, abdominal pain in 25%, and a palpable mass in abdominal cavity - 23%, shortness of breath - in 20%, ataxia - in 15% and diarrhea - in 15% of cases. The relatively low incidence of vomiting and abdominal pain is particularly noteworthy, as these are the most common clinical symptoms of pancreatitis in dogs and humans. In addition, clinical symptoms such as polyphagia, constipation, fever, icterus, polyuria, polydipsia and adipsia were observed in cats. Often pancreatitis was accompanied by hepatic lipidosis, inflammatory bowel disease, interstitial nephritis, diabetes mellitus and cholangiohepatitis.

Detailed clinical and biochemical blood tests often reveal only weak and nonspecific changes. Serum lipase and amylase activities are within normal limits in most cases. In some cases, x-rays show a weakening of the contrast of the cranial abdominal cavity, as well as a displacement of the duodenum laterally and dorsally, the stomach to the left, and the colon caudally. Ultrasound examination of the abdominal organs is very helpful in making a diagnosis. Among the observed changes, it is worth noting swelling of the pancreas, its hyperechogenicity, accumulation of fluid around it and, which is rare, the presence of a neoplasm in the pancreas area. Computed tomography of the abdomen is a common procedure in the evaluation of people with suspected pancreatitis, and although it can be quite useful in diagnosing pancreatitis in cats, this method is currently used very rarely.

In order to diagnose feline pancreatitis, the authors' laboratory tested a radioimmunoassay to measure serum trypsin-like immunoreactivity. Initial data suggested that most cats with pancreatitis have increased immunoreactivity. In the future, analysis of trypsinogen activation peptide and trypsin agprotease inhibitory complex may be useful for diagnosis.

The definitive diagnosis can be made based on a biopsy of the pancreas during exploratory laparotomy or laparoscopy. Although the biopsy itself is quite safe, the procedure is expensive and may also be contraindicated in some animals due to the high risk associated with anesthesia.

Treatment

Maintenance therapy
It is necessary to eliminate the main cause of pancreatitis, if possible. The use of unnecessary drugs, especially those that can cause pancreatitis, should be suspended. The main supportive method is active infusion therapy. In addition, it is necessary to correct the water, electrolyte and acid-base balance as soon as possible.

Nutrition
Traditional recommendations for any animal with pancreatitis are that nothing should be administered orally for 3-4 days. This is quite reasonable for animals in which pancreatitis is accompanied by vomiting, but is a very controversial issue for those who do not vomit. This problem is complicated by the fact that cats with pancreatitis often have hepatic lipidosis. The authors believe that the proven benefits of feeding cats with hepatic lipidosis outweigh the recommendation not to feed the animal. The preferred method of feeding is a jejunostomy feeding tube. However, in many cases, its installation is difficult, so you should use a gastrostomy or even a nasogastric tube - of course, if the animal is not vomiting. If the cat is vomiting and does not have signs of concomitant liver lipidosis, then nothing should be given orally for 3-4 days. After this period, you can begin to gradually give water, and then switch the animal to feed with a high carbohydrate content and low fat content in small portions (for example, PurinaCNMO-formula or Hill'sfelinei/d). A similar diet is also suitable for tube feeding, as shown in Table 1.

Analgesic drugs
Although abdominal pain is not very common in cats with pancreatitis, you should carefully monitor the animal for any discomfort. If this is the case, then it is necessary to prescribe analgesic drugs. Meperidine (Demerol) at a dose of 1-2 mg/kg every 2-4 hours can be administered intramuscularly or subcutaneously. You can also use butorphanol tartrate (Torbutrol or Torbujesic) at a dose of 0.2-0.4 mg/kg every 6 hours s.c.

Treatment with plzma
Studies conducted on dogs suggest that when α 2 -macroglobulin, one of the proteins that clears the serum of activated protease, is depleted, the animal quickly dies. Fresh frozen plasma (FFP) or fresh whole blood contains not only (α2-macroglobulins, but also albumins, which are very beneficial for animals with pancreatitis. Unfortunately, clinical trials conducted in humane medicine have not revealed a beneficial effect of plasma. But based on our own experience of the authors and not very reliable reports on the benefits of FFP for dogs with pancreatitis, both FFP and fresh whole blood can be recommended for the treatment of cats with severe pancreatitis.

Antibiotic therapy
The conventional recommendation to use antibiotics to treat cats with pancreatitis is based on nothing. Although some recent papers have suggested a reduction in human mortality with early use of antibiotics, a closer look at these data reveals that antibiotic treatment helped only a very small number of patients - those with infectious complications. Based on necropsy results, infectious complications in cats are very rare, so the authors do not recommend the use of antibiotics unless the cause of the infectious complication is clearly known.

Anti-inflammatory drugs
There are no data on the use of anti-inflammatory drugs in cats with severe pancreatitis. They did not bring any benefit to sick people. Therefore, when treating cats with severe pancreatitis, corticosteroids should be used only in cases of secondary cardiovascular shock. However, they can be used to treat inflammatory bowel disease and associated low-grade chronic pancreatitis, since these drugs do not appear to have adverse effects in such pathologies.

Dopamine
Dopamine has been shown to be effective in treating cats with experimentally induced pancreatitis, but only when administered within the first 12 hours of disease onset. Additionally, caution should be used when treating patients with cardiac arrhythmias with dopamine. And because it can also cause nausea, vomiting and seizures, it is not recommended for use as a common treatment for pancreatitis in cats.

Other healing methods
Methods such as trypsin inhibitors (eg, Trasylol), antacids, antisecretory agents (including anticholinergics, calcitonin, glucagon, somatostatin), selenium, and peritoneal lavage have been used in the treatment of people with pancreatitis (see previous article ). But none of these, with the exception of selenium supplementation, have been shown to be effective and should therefore be avoided. By the way, the benefits of selenium were also discovered in the treatment of cats.

It should be remembered that many cats have a moderate form of chronic pancreatitis. Concomitant diseases, such as inflammatory bowel disease, are also common. Little is known about the treatment of such animals, so it is often limited to the treatment of concomitant diseases and careful monitoring of the progression of pancreatitis.

Forecast
The prognosis for cats with severe pancreatitis directly depends on the severity of the disease, the extent of pancreatic tissue necrosis, the presence of systemic and pancreatitis complications, the duration of this condition and the presence of concomitant diseases.

Exocrine pancreatic insufficiency

Exocrine pancreatic insufficiency (EPI) is a syndrome caused by insufficient secretion of digestive enzymes by the exocrine pancreas, which leads to insufficient activity of these enzymes in the lumen of the small intestine.

Etiology and pathogenesis
In cats, as in humans, the most common cause of EPI is chronic pancreatitis. Other reasons are infestation Eurytremaprocyonis and idiopathic acini atrophy. After the onset of clinical symptoms, the basic functional abilities of the exocrine pancreas are lost. The lack of digestive enzymes in the duodenum leads to poor digestion of food. In addition, problems arise with the transport mechanisms of the intestinal mucosa. All these changes lead to the formation of copious soft stools, steatorrhea and weight loss. Reduced fat absorption can lead to a deficiency of fat-soluble vitamins.

Clinical picture and diagnosis
Cats with EPI experience chronic polyphagia, diarrhea, and weight loss. High fat content in feces can lead to a deterioration in the appearance of the coat (greasy hair), especially in the crotch and tail areas. At the same time, clinical and biochemical blood tests and urine tests are almost always within normal limits. In most cases, X-ray and ultrasound examinations of the abdominal cavity do not reveal any abnormalities. The most reliable test for diagnosing EPI in cats is a radioimmunoassay to measure serum trypsin-like immunoreactivity. The reference range is 17 to 49 mcg/L, and if EPI is present, the value is 8 mcg/L or less. Cats with EPI are usually depleted of cobalamin and, less commonly, folate. Therefore, if EPI is suspected, the level of cobalamin and folate in the blood serum should be determined.

Treatment

Pancreatic Enzyme Supplements
As with dogs, pancreatic enzyme supplements are the primary treatment for cats with EPI. For this, dry powder extract of bovine or pork pancreas can be used. First, 1 teaspoon is mixed with food and applied 2 times a day (Viokaz or Pancrezim). If the cat refuses to eat this mixture, then the dry preparation can be placed in a gelatin capsule or the animal can be offered raw beef or pork pancreas. Initially, at each feeding, 30-90 g of chopped raw pancreas is given (it can be stored frozen for a long time without loss of enzyme activity). If the cat refuses this too, you should prepare a liquid fish-based supplement - most cats eat this with pleasure. Tablets, capsules and other similar products should be avoided. Pre-incubating the feed with pancreatic enzymes in a thermostat, adding bile salts, or using concomitant antacid therapy is not necessary. After elimination of clinical symptoms, the dose of pancreatitis extract can be gradually reduced to the minimum effective. The latter varies depending on the individual characteristics of the cat and the type of supplement.

Some nuances of diet therapy
Unfortunately, enzyme supplements are not able to normalize the absorption of fats. The fact is that some of the lipases they contain are irreversibly denatured by the low pH level in the cat's stomach. Low-fat food further deprives the animal of essential fatty acids and fat-soluble vitamins and should therefore be avoided. Because some types of dietary fiber can interfere with pancreatic enzyme activity, high fiber foods should also be avoided. Cats with EPI require a special, high-quality maintenance diet.

Vitamin supplements
In most cases, EPI is accompanied by cobalamin deficiency. Some cats respond poorly to enzyme supplemented treatments until cobalamin is added. Initially, 100-250 mcg of cobalamin should be injected subcutaneously once a week (cyanocobalamin injection), and after 2 months its serum concentration should be measured. If the level has returned to normal, then injections should be performed once a month, then once every two months and finally once every six months. In this case, the concentration of cobalamin and folate in the blood serum should be measured annually.

Treatment of concomitant diseases
Fat-soluble vitamin deficiencies are uncommon but should be considered as a possible complication. Vitamin K deficiency can be especially life-threatening. Some cats with EPI do not respond adequately to cobalamin enzyme supplements. Most have inflammatory bowel disease, which is evidence of decreased serum folate concentrations. Finally, some cats develop diabetes mellitus, which also requires treatment.

Forecast
In most cases, EPI causes irreversible destruction of the pancreatic acini, so complete recovery is unlikely. However, with appropriate treatment and observation, such animals usually quickly gain weight, their stool returns to normal, and they can continue to live a full life.

Exocrine neoplasms of the pancreas

Pancreatic adenomas are benign tumors of the exocrine pancreas. Pancreatic adenocarcinoma is the most common pancreatic malignancy in cats. In addition, several cases of spindle cell sarcoma and lymphosarcoma have been reported.

Pathogenesis
Pancreatic adenomas usually have a subclinical course, but can cause the development of clinical symptoms due to displacement of abdominal organs. In addition, such adenomas can lead to pancreatic duct obstruction, acini atrophy, as well as tumor necrosis, followed by clinical symptoms of pancreatitis and those clinical symptoms that are caused by malfunction of other organs as a result of metastasis.

Clinical symptoms and diagnosis
Clinical signs of exocrine pancreatic neoplasms in cats are not specific. In a study of 58 cases, the most common clinical symptoms were anorexia (46%), weight loss (37%), lethargy (28%), vomiting (23%), jaundice (14%), constipation (9%) and diarrhea (3). %). Other clinical symptoms included polyuria, steatorrhea, fever, dehydration, and cranial abdominal distension. In addition, symptoms associated with metastasis may occur, such as shortness of breath, claudication, bone pain, or alopecia.

Routine blood tests are usually inconclusive. Serum lipase and amylase activity was reported in only a few cases, and even more rarely was the activity elevated. In most cases, X-ray examination is nonspecific, and therefore it is better to resort to ultrasound examination of the abdominal organs. A soft tissue mass can usually be found in the pancreatic area, but the relationship with pancreatic tissue can rarely be demonstrated conclusively. Although most pancreatic adenocarcinomas exfoliate a small number of cells into the peritoneal fluid, if an effusion is present, it should be aspirated and subjected to cytological examination. If it is necessary to study the neoplasm, one should resort to aspiration of its contents with a thin needle or percutaneous biopsy under ultrasound guidance. However, the absence of cell detachment may result in a negative result when using the fine needle aspiration method. In most cases, the final diagnosis is made on the basis of exploratory laparotomy or even necropsy.

Therapy and prognosis
Pancreatic adenomas are benign and theoretically do not require treatment until they cause clinical symptoms. However, the final differential diagnosis between an adenoma and adenocarcinoma of the pancreas can often be made only with diagnostic laparotomy and at the same time partial pancreatectomy. If this study confirms the presence of pancreatic adenoma, the prognosis will be favorable.

Pancreatic adenocarcinoma often occurs at an advanced stage of the disease, with metastases occurring in 81% of cats diagnosed. If no metastatic spread is observed at the time of diagnosis, surgical resection of the adenocarcinoma should be considered. However, the animal owner should be immediately warned that this operation is rarely completely successful. Total pancreatectomy and pancreaticoduodenectomy are theoretically possible, but have not been reported in cats at the time of this writing. Extrapolation from experimental animal and human data suggests that these procedures are associated with high morbidity and even mortality. In addition, the complex, postoperative, lifelong treatment of EPI and diabetes mellitus makes this procedure highly undesirable. Chemotherapy or radiation therapy used to treat pancreatic adenocarcinomas in humans and animals has little success. Thus, the prognosis for cats with adenocarcinoma is fatal.

Pancreatic bladder

The pancreatic bladder is a pathological dilation of the pancreatic duct, shaped like a sac. Only a few cases of this phenomenon in cats have been described in the veterinary literature. They experienced clinical symptoms comparable to those encountered with bile duct obstruction. The necessary treatment has not yet been found, but if clinical symptoms are present, surgical intervention can be resorted to.

A pancreatic pseudocyst is a collection of sterile pancreatic juice surrounded by fibrous or granulation tissue. In humans, it is considered a complication of pancreatitis, and not so long ago it was found in cats. Clinical signs of pseudocysts were similar to those seen in cats with pancreatitis. An abdominal ultrasound examination revealed a cystic mass in close proximity to the left lobe of the pancreas. In humans, pancreatic pseudocyst is treated surgically, but only if it does not decrease in size or, on the contrary, increases. In the case mentioned, surgery was also successful in treating this cat.

Pancreatic abscess

A pancreatic abscess is a collection of pus with little or no tissue necrosis, most often in close proximity to the pancreas. In humans and dogs it is considered a complication of pancreatitis, but this is not the case in cats. However, the authors are aware of one clinical case in which a pancreatic abscess was confirmed by histopathological examination in one cat. Treatment of pancreatic abscess in humans and dogs involves surgery and aggressive antibiotic therapy. Using the same means, we were able to achieve success in treating the previously mentioned cat.

Pancreatic function

The pancreas is a small, light pink glandular organ located under the stomach along the duodenum. The pancreas secretes a number of hormones, in addition, the exocrine zones of the gland secrete enzymes that help digest food. Without enough digestive enzymes in exocrine pancreatic insufficiency, nutrients from food cannot be digested and absorbed. As a result, weight loss or chronic diarrhea (diarrhea) of gray fecal matter develops, or both symptoms occur. Dogs often have dull coats with a lot of dander, and coprophagia (eating their own feces) may occur.

In dogs This disease is not a congenital pathology, but there is a genetic predisposition. Probably, in this case there is an autosomal recessive mode of inheritance. The pathogenesis (mechanism of development) of the disease includes autoimmune destruction of pancreatic tissue and atrophy of the acini. The affected areas of the gland decrease in size and cease to function.

Exocrine pancreatic insufficiency in dogs can develop at any age, but is more common in dogs under 4 years of age. German Shepherds and Rough Collies are predisposed to this disease. According to statistics, 70% of dogs with exocrine pancreatic insufficiency are German shepherds, and 20% are rough collies.

In cats The cause of the disease is usually pancreatitis. no genetic inheritance has been identified.

Abroad, and today in our clinic, for this purpose, first of all, TLI is used - a test for trypsin immunoreactivity in blood serum. In addition, a fecal elastase ELISA test may be used. Both of these tests are species specific. Also, to diagnose pancreatic insufficiency, the doctor uses as much data as possible about the animal, taking into account its breed, age, symptoms, data on the presence of the disease in the parents, and fecal analysis for feed digestibility.

Therapy consists of prescribing pancreatic enzymes. The drugs are given to animals with food; the action of powdered drugs is more effective than tablets. It has been proven that enzymes must be given directly during feeding.

In some animals, a good therapeutic effect is observed with the combined use of enzymes and antisecretory drugs (H2-histamine receptor blockers), which reduce the production of hydrochloric acid in the stomach, and thereby protect enzymes from the action of gastric juice. Proton pump blockers (omeprazole, etc.) can be used for the same purpose.

Patients with pancreatic insufficiency require dietary nutrition. The best diet is easily digestible food. Such foods are low in fiber and fat, which is especially important for animals with low weight.

Since in pancreatic insufficiency most nutrients are not absorbed into the blood, they are actively consumed by intestinal microorganisms. As a result, the bacterial population grows progressively. This process negatively affects the health of the animal. One of the consequences is vitamin B12 deficiency, due to which a clinical picture of anemia and neurological disorders can develop. At the beginning of treatment, a course of antibiotic therapy is recommended, followed by periodic injections of vitamin B12. In some cases, additional administration of vitamins E and K 1 is necessary.

Treatment must be continued throughout the animal's life. If you stop administering enzymes, the symptoms of the disease will return again. A positive response to treatment is an improvement in condition one week after starting it.

The described treatment tactics are usually very effective. But it is important to know that:

In approximately one dog in five, treatment may be unsuccessful,

Most animals never gain normal weight.

In such cases, it is important to ensure that other diseases that may accompany pancreatic insufficiency (bacterial overgrowth) or cause similar symptoms (eg, inflammatory bowel disease, infiltrative enteritis) have been excluded. In some cases, this requires a biopsy of the intestines and pancreas.

anesthesiologist-resuscitator

Pancreatic function

Exocrine pancreatic insufficiency

In dogs This disease is not a congenital pathology, but there is a genetic predisposition. Probably, in this case there is an autosomal recessive mode of inheritance. The pathogenesis (mechanism of development) of the disease includes autoimmune destruction of pancreatic tissue and atrophy of the acini. The affected areas of the gland decrease in size and cease to function.

In cats The cause of the disease is usually pancreatitis, no genetic inheritance has been identified.

Diagnostics

Treatment

The described treatment tactics are usually very effective. But it is important to know that:

In approximately one dog in five, treatment may be unsuccessful,

Most animals never gain normal weight.

ETIOPATHOGENESIS AND FEATURES:

Characteristics.
The pancreas, due to its complex anatomical location, is difficult to use with conventional physical methods of examination.
Its condition can only be judged by the dysfunction of other organs associated with it.
Insufficiency of gland function can manifest itself both in a lack of enzymes and in the inability of digestive juice to maintain an alkaline pH in the intestines.
Under these conditions, normal intestinal cavity digestion is disrupted, microbes multiply intensively in the small part, and intestinal dysbiosis occurs, further worsening the digestive processes.
Parietal enzymatic digestion (maldigestion syndrome) and absorption of enzymatic hydrolysis products (malabsorption syndrome) are disrupted.
Exhaustion increases with increased appetite (malnutrition syndrome), and the function of other endocrine glands is disrupted.

ETIOLOGY:
Exocrine pancreatic insufficiency (EPI) can be caused by pancreatic disease or pancreatic failure. Further changes are the result of a disease process that affects the regulation of pancreatic secretion and the activity of pancreatic enzymes.
Functional exocrine apancreatic insufficiency can be defined as exocrine pancreatic insufficiency not caused by morphological disease of the pancreas.
Duodenal mucosal disease (DMD). It provokes EPN through the following mechanism: the hormones cholecystokinin and secretin are synthesized in the duodenum, which cause and stimulate pancreas secretion.
The duodenal mucosa also has receptors, the irritation of which causes the release of these hormones. DMB also reduces the synthesis and release of the enzyme endocrinase, which activates trypsin by pripsinogen, and activation of trypsin plays a major role in the activation of all pancreatic proteases.

Causes of deficiency of pancreatic enzyme activity in the intestines:

1. INADEQUATE SECRETION OF THE PANCREAS:
Decreased pancreatic synthesis
Pancreas atrophy;
Congenital enzyme deficiency;
Decreased secretion of the normal pancreas
Duodenal mucosal disease
Nervous regulation disorders
Humoral regulation disorders
Slow secretion of normal pancreas. glands
Duodenal mucosal disease

2. REDUCED ENZYME ACTIVITY:
Duodenal mucosal disease
Enterokinase deficiency
Lack of bile acids
Decreased lipase activity
Reduced trypisinogen activity due to enterokinase.

3. INTESTINAL FACTORS DECREASING ENZYME ACTIVITY:
Extremely acidic optimum pH activity
Low gastric emptying rate
Duodenal mucosal disease
Affected by enterogastron-mediated reflex
Affected by the enterogastric reflex
Overfeeding
Decreased level of pancreatic secretion
Deficiency of bicarbonate secretion
Reduced level of proteolytic breakdown of enzymes
Bacterial proteases
Hyperreproduction of microflora caused by:
Stasis
Obstruction
Hypomobility

PATHOGENESIS:
the mucous membrane of the small intestines (especially the duodenum) synthesizes the hormones cholecystokinin and secretin, which stimulate pancreatic secretion. There are receptors in the mucosa that help the release of these hormones. The duodenal mucosa has a very high concentration of receptors and endocrine secretory cells, but pancreatic secretion can also be simulated by jejunal hormones. Any chronic mucosal disease therefore inhibits the secretion of pancreatic products.
Their increased degradation by digestive enzymes has a similar effect. This occurs when proteases that are destroyed are in deficiency due to mucosal atrophy or other pathology, which makes them active and they inactivate pancreatic enzymes that are secreted in sufficient quantities.

FEATURES: chronic pancreatitis and juvenile pancreas atrophy -
- the most common causes of exocrine pancreatic insufficiency.

Summary clinic:
1. Anorexia (lack of appetite, refusal to eat);
2. Tousled fur;
3. Diarrhea;
4. Exhaustion, cachexia, unkemptness;
5. Unusual or foul-smelling stool;
6. Polydipsia, increased thirst;
7. Polyphagia, extremely increased appetite;
8. Loss of body weight;
9. Vomiting, regurgitation, emesis;
10. Steatorrhea, fat in stool;
11. Enlarged borborygms, flatulence;
12. Depression (depression, lethargy);
13. Flatulence;

Symptoms Endocrine pancreatic insufficiency is characterized by: polydipsia and polyuria, vomiting, flatulence (discharge of foul-smelling gases), pancreatogenic diarrhea (smelly, with frequent bowel movements and an increase in the volume of feces, not amenable to therapy), pancreatogenic stool (polyfecal - bulky stool in the form of foamy, soft, spongy colorless masses with a sour odor, a greasy sheen and undigested food debris, sometimes mixed with blood), polyphagia up to coprophagia, flatulence in all parts of the intestine, hyperglycemia, glucosuria, hypocholesterolemia, increased amylase levels in the blood serum, steatorrhea, creatorrhoea, amilorrhea, acidity feces.

Diagnosis: based on:
- clinical signs;
- examination of feces for the presence of traces of muscle fibers;
- examination of feces for the presence of fats;
- tests for the level of protein processing;
- BT-PABA tests;
- 72-hour fecal tests for fats or serum trypsin-like immunoreactivities measured by radioimmunoassays;
- influence of exposure to pancreatic enzymes;

It is not always possible to make a diagnosis while the animal is alive.
If the listed symptoms are detected during examination, there is reason to suspect pancreaopathy.
Ascites in combination with hyperglycemia also indicates the participation of the pancreas in the pathological process.
To be more confident in making a diagnosis, one or two functional tests are performed.

Differential diagnosis.
Symptoms of exocrine pancreatic insufficiency must be distinguished from polyphagia caused by chronic enteritis and various types of malabsorption.
Pancreaopathy is characterized by polyphagia against a background of progressive cachexia. The activity and performance of the animal can be maintained for a long time, which is not typical for chronic enteritis and hepatopathy (rapid increase in depression, temporary or long-term loss of appetite).
Pancreaopathy is also distinguished by concomitant bradycardia; in contrast to enterocolitis, defecation is frequent, but there is no tenesmus.

TREATMENT, DEVELOPMENT AND PROGNOSIS:

MEDICATION:
- Mezim forte: 1-2 tblt/day for 5-7 days;
- Trizim: 1-2 tblt/day for 5-7 days;
- Cimetidine: 5-10 mg/kg/8 hours/per os;
- Neomycin (Neomicin) sulfas: 2.5-10 mg/kg/per os/6-12 hours;

Additional - symptomatic:
- Spasmolyt: initially once 1 ml/10 kg/iv;

DEVELOPMENT: acute, with a tendency to become chronic.

FORECAST: doubtful to favorable.