Pancreatic disease Flashcards
What are the main digestive enzymes produced by the pancreas?
In addition to the proteases, lipase and amylase, the pancreas produces a host of other digestive enzymes, including ribonuclease, deoxyribonuclease, gelatinase and elastase.
What is a zymogen and why are these especially important in the pancreas?
An inactive substance which is converted into an enzyme when activated by another enzyme
The pancreas secretes zymogens partly to prevent the enzymes from digesting proteins in the cells in which they are synthesised.
Enzymes like pepsin are created in the form of pepsinogen, an inactive zymogen.
Discuss neutralisation of duodenal juice with HCO3-, Cl- and water
In the duodenum, gastric acid is neutralized by sodium bicarbonate. This also blocks gastric enzymes that have their optima in the acid range of pH. The secretion of sodium bicarbonate from the pancreas is stimulated by secretin. This polypeptide hormone gets activated and secreted from so-called S cells in the mucosa of the duodenum and jejunumwhen the pH in the duodenum falls below 4.5 to 5.0. The neutralization is described by the equation:
HCl + NaHCO3 → NaCl + H2CO3
The carbonic acid rapidly equilibrates with carbon dioxide and water through catalysis by carbonic anhydrase enzymes bound to the gut epithelial lining, leading to a net release of carbon dioxide gas within the lumen associated with neutralisation. In the absorptive upper intestine, such as the duodenum, both the dissolved carbon dioxide and carbonic acid will tend to equilibrate with the blood, leading to most of the gas produced on neutralisation being exhaled through the lungs.
Why is cobalamin important?
Cobalamin: Also called vitamin B12. A vitamin important for the normal formation of red blood cells and for the health of the nerve tissues. Undetected and untreated vitamin B12 deficiency can lead to anemia and permanent nerve and brain damage.
What might happen if normal bacterial flora is disrupted in the GI tract?
Risk for microbial infection
Signalment: 5 year old MN Labrador
Relevant history: 8-10 month history of chronic progressive diarrhoea which started intermittent and is now more persistent. He has a ravenous appetite with pica at times. He is prone to scavenging and occasionally vomits (once or twice a month).
He passes large volumes of steatorrhoeic foul smelling diarrhoea 2-3 times a day. There is no dyschezia, haematochezia or urgency. The owners have not seen any mucus. He frequently has boroborygmi and flatulence.
How would you categorise Bertie’s diarrhoea?
Chronic
Signalment: 5 year old MN Labrador
Relevant history: 8-10 month history of chronic progressive diarrhoea which started intermittent and is now more persistent. He has a ravenous appetite with pica at times. He is prone to scavenging and occasionally vomits (once or twice a month).
He passes large volumes of steatorrhoeic foul smelling diarrhoea 2-3 times a day. There is no dyschezia, haematochezia or urgency. The owners have not seen any mucus. He frequently has boroborygmi and flatulence.
How would you categorise Bertie’s diarrhoea?
Chronic
Previous management tried by numerous vets…
Diet trials: the following diets have all been tried (individually) for periods of 3-8 weeks
Home cooked chicken and rice for 3 weeks: some improvement in faecal consistency
Commercial ocean fish and rice diet: no improvement
Royal Canin low fat sensitivity control diet formulated for GI disease: some improvement
Purina hypoallergenic HA diet: some improvement-variable stool consistency
What do you need to know about how these diet trials were conducted in order to decide what they can and can’t rule out?
What else was fed?
How was it fed?
What was in the food? Rule out allergy
Signalment: 5 year old MN Labrador
Relevant history: 8-10 month history of chronic progressive diarrhoea which started intermittent and is now more persistent. He has a ravenous appetite with pica at times. He is prone to scavenging and occasionally vomits (once or twice a month).
He passes large volumes of steatorrhoeic foul smelling diarrhoea 2-3 times a day. There is no dyschezia, haematochezia or urgency. The owners have not seen any mucus. He frequently has boroborygmi and flatulence.
How would you categorise Bertie’s diarrhoea?
Chronic
Previous management tried by numerous vets…
Diet trials: the following diets have all been tried (individually) for periods of 3-8 weeks
Home cooked chicken and rice for 3 weeks: some improvement in faecal consistency
Commercial ocean fish and rice diet: no improvement
Royal Canin low fat sensitivity control diet formulated for GI disease: some improvement
Purina hypoallergenic HA diet: some improvement-variable stool consistency
What do you need to know about how these diet trials were conducted in order to decide what they can and can’t rule out?
What else was fed?
How was it fed?
What was in the food? Rule out allergy
Other treatments Bertie has had:
5 day course of fenbendazole: no improvement
Would this treatment rule anything out- if so, what?
Is this treatment trial justified?
Yes would rule out malabsorbtion due to GI parasites
Signalment: 5 year old MN Labrador
Relevant history: 8-10 month history of chronic progressive diarrhoea which started intermittent and is now more persistent. He has a ravenous appetite with pica at times. He is prone to scavenging and occasionally vomits (once or twice a month).
He passes large volumes of steatorrhoeic foul smelling diarrhoea 2-3 times a day. There is no dyschezia, haematochezia or urgency. The owners have not seen any mucus. He frequently has boroborygmi and flatulence.
How would you categorise Bertie’s diarrhoea?
Chronic
Previous management tried by numerous vets…
Diet trials: the following diets have all been tried (individually) for periods of 3-8 weeks
Home cooked chicken and rice for 3 weeks: some improvement in faecal consistency
Commercial ocean fish and rice diet: no improvement
Royal Canin low fat sensitivity control diet formulated for GI disease: some improvement
Purina hypoallergenic HA diet: some improvement-variable stool consistency
What do you need to know about how these diet trials were conducted in order to decide what they can and can’t rule out?
What else was fed?
How was it fed?
What was in the food? Rule out allergy
Other treatments Bertie has had:
5 day course of fenbendazole: no improvement
Would this treatment rule anything out- if so, what?
Is this treatment trial justified?
Yes would rule out malabsorbtion due to GI parasites
2 week course of enrofloxacin: if anything a bit worse
Would this treatment rule anything out- if so, what?
Is this treatment trial justified?
Not justified as there are no clinical signs to suggest needing antimicrobial… e.g. blood in poop
4 week course of prednisolone: Bertie’s diarrhoea was the same and he was even more ravenous and therefore scavenged even more. He was also polydipsic and seemed to lose more weight.
Would this treatment rule anything out or make anything less likely- if so, what?
Why did Bertie seem to lose more weight despite eating even more?
Help to rule out IBD or inflammatory conditions.
Increased metabolic rate = weight loss
Physical Examination:
BCS 1/5, generalised muscle wasting and dry seborrheic coat. TPR normal, no evidence of dehydration, mucous membranes pink. Abdominal palpation suggests soft intestinal contents. No abnormalities detected and very easy to palpate due to body condition. Thoracic auscultation normal. Peripheral LNs all seem normal/not enlarged.
You decide to run some blood and urine tests:
Haematology: Blood smear: red cells appear normochromic and normocytic, white cells unremarkable, plenty of platelets
Clinical biochemistry: Raised ALT, ALP and lowered Calcium and cholesterol.
Urinalysis: free catch sample. SG >1.040, dipstick normal.
ELISA for giardia: -ve
Zinc sulphate flotation test: no parasites seen
Can you explain all the blood results?
Modest increases in Serum alanine aminotransferase (ALT) and a decrease in cholesterol concentration are seen on routine biochemical studies in some dogs. Serum concentrations of cobalamin may be low whilst serum folate concentrations may be high. Low serum concentrations of Vitamin E are also frequently documented in dogs with EPI. The most sensitive and specific test for the diagnosis of EPI is the TLI serum assay. The values are greatly reduced as compared to normal animals. Values <2µg/l in dogs are considered diagnostic. This test must be carried out after withdrawing food for several hours
Anaemia – due to low B12.. (would normally expect macrocytic)- could be there are no gross changes yet.
What is your diagnosis?
EPI
How does the sensitivity and specificity of one of the tests help you be confident in your diagnosis?
The most sensitive and specific test for the diagnosis of EPI is the TLI serum assay
What underlying pathological disease processes can cause EPI in dogs?
EPI is due to pancreatic acinar atrophy (PAA) in approximately 50% of cases
Dogs with EPI attributable to PAA are typically young adults (1–2 years of age). Dogs with EPI due to chronic pancreatitis are often middle-aged to older but can be of any age.
Come up with a management plan for Bertie?
- How will you monitor his progress?
- TREATMENT
- Inpatient or Outpatient
- Outpatient medical management should be directed toward replacement of pancreatic digestive enzymes and cobalamin supplementation when necessary.
- Inpatient treatment may be necessary in dogs with concurrent diabetes mellitus that require insulin therapy.
- Treatment of choice includes providing digestive enzymes with each meal.
- Medical (also see Medications)
- Digestive enzyme replacement
- ►Treatment of choice includes providing digestive enzymes with each meal.6
- ►Powdered pancreatic enzyme supplements of porcine or bovine origin are mixed with the diet (initially 1 tsp/10 kg body weight with each meal mixed into the food immediately before feeding). After a complete response, this dose can usually be significantly decreased.
- ►Tablets, capsules, and enteric-coated preparations are less effective in dogs.
- ►Preincubation of the diet with the enzyme supplement or addition of antacids or bile acids is not necessary.
- ►Enzyme activity may vary with the product used and also within containers.
- ►A strong body odor has been anecdotally reported in some dogs treated with replacement enzymes.
- ►Some dogs may develop oral bleeding, which often resolves after the dose of enzymes is lowered.
- Cobalamin should be supplemented if the patient is cobalamin deficient.
- ►Cobalamin must be administered parenterally (usually given by subcutaneous injection).
- ►Pure cyanocobalamin should be used.
- • Dose is 250 to 1200 mcg per injection, depending on the size of the dog.
- • Initially given once a week for 6 weeks, then 1 more dose 30 days later; serum cobalamin concentration is rechecked 30 days after that.
- • Some dogs need only short-term cobalamin supplementation; others require lifelong supplementation.
- cTLI = canine trypsin-like immunoreactivity, EPI = exocrine pancreatic insufficiency, GI = gastrointestinal, PAA = pancreatic acinar atrophy
- Nutritional
- Maintenance diets or light maintenance diets fed twice daily usually work well.
- High- or low-fat and high-fiber diets should be avoided.
