Nutritional Managmement of Gastrointestinal Disease, Pancreatic Disease, and Dermatological Disease

Question 1

What is the organ that is most affected by nutrition? What do the enterocytes rely on within the intestinal lumen for sustenance? What is the importance of protein, and what is produced as a result that is essential?

Answer 1

The organ system most affected by nutrition
The enterocytes rely on nutrients in the intestinal lumen
- Protein: source of essential amino acids, dispensable amino acids for oxidation, AA and
energy for microflora
- Key for hormone stimulation (insulin, IGF-1, GLP-2, CCK)
antigenicity

Question 2

What is glutamine? Arginine? Where is fat absorbed and what does it stimulate/ cause?

Answer 2

• Glutamine: fuel source for mucosal lymphocytes
• Arginine: metabolized to NO
• Fat: absorbed through the lymphatics, stimulates CCK, peptide YY, GLP-1
• Slows GI motility
• Butyrate: fuel source for colonocytes, anti
  inflammatory
• Fiber: soluble and insoluble

Question 3

What are the clinical signs of pets with GI disease?

Answer 3

 Loss of appetite - or ravenous appetite
 Weight loss
 Abdominal pain/discomfort (can have gas pain/ discomfort, gi distention)
 Small bowel diarrhea
- Voluminous
- Low urgency
- No mucus
- No tenesmus
 Large bowel diarrhea
- Low volume
- Mucus
- High urgency
- Tenesmus

Question 4

What is B12 and Folate?

Answer 4

 Cobalamin (B12):
- Absorbed in the distal small intestine (specifically in the ileum)
- Values below the control range:
- EPI & bacterial overgrowth in the small intestine  diseases affecting the distal small intestine (such as IBD)
 Folate (B9) :
- Absorbed in the proximal small intestine
- Values above the control range:
- bacterial overgrowth in the small intestine  Values below the control range:
- disease affecting the proximal small intestine

Question 5

What can be the results of adverse reactions to food?

Answer 5

Inappropriate immune response to dietary antigen
 Local cell mediation inflammation, may lead to IBD
 Local antibody production (non-IgA). IgE may lead to mast cell stimulation
 Systemic IgE production (dermatological signs? Other)

Question 6

What are potential contributing factors to adverse reactions to food?

Answer 6

 Potential contributing factors:
 Bacterial enterotoxins
 Parastism
 Malnutrition

Question 7

What is IBD? Is IBD a specific disease? What is its characteristics? What must you rule out?

Answer 7

IBD is a histopathological definition; often misused to describe all-cause chronic enteropathy

Not a single entity

 Characterized by infiltration of immune cells to the lamina propria

 Rule outs- parasites, bacterial enteritis/ dysbiosis, dietary intolerance, neoplasia

Question 8

What are the possible consequences of chronic enteritis?

Answer 8

 Protein-energy malnutrition (poor body condition scores, hypoabuminemia, ascites)

 Hypomagnasemia

 Anemia/ iron deficiency

 Cobalamin and folate deficiency

 Vitamin K deficiency ( can cause bleeding, inhibition of formation of some clotting factors)

 Antioxidant deficiencies (zinc, vitamin E, riboflavin)

(they will sometimes present like a hypocalecemic patient)

 Vitamin D and calcium deficiency

 Dysbiosis

Question 9

What is the cause of lymphangiectasia? What is the potential consequences of it? What is the treatment?

Answer 9

 Can be a result of mucosal inflammation, extraluminal obstruction, intraluminal adhesions

 Leads to panhypoproteinemia, hypocholesterolemia, lymphopenia

 Treatment:
 Fat restriction- relieves lymphatic pressure

 Medium chain triglycerides- generally not recommended

 Elemental diets- temporarily

Question 10

What are different nutrient strategies utilized for patients with chronic enteropathies?

Answer 10

 Fiber supplementation (soluble fiber as prebiotics, insoluble helps motilityconsistency)/probiotics (adding fiber can decrease digestibility, so it can worsen maldigestive disorders)

 Provision of antioxidants

 Correction of hypomagnesemia, supplementation of vitamin K

 Moderate fat/ fat restriction- may improve clinical signs in several ways

 Omega-3 PUFA  High digestibility

 Reducing antigenicity
 Novel protein: diet Hx!

 Hydrolyzed protein

Question 11

What is the difference between acute and chronic colitis?

Answer 11

Acute

 Caused by ingestion of foreign material, specific pathogens

 Changes in intestinal peristalsis

 Lack of evidence-based approach for management

 Highly digestible diet/fiber responsive?

 Prebiotics?

Chronic

Same reasons/management as acute
+ Food antigenicity

 Novel protein

 Omega-3

Question 12

Is chronic GI signs easily treated?

Answer 12

No, not every patient responds to the same thing and make judgements/ decisons based on history and the patient. There is no fix all, and it requires alot of trial and error

Question 13

What are some different histories prior to gi incidence and what it will indicate?

Answer 13

History of fat intolerance? Try low fat

History of ‘ingredient sensitivity’? Try novel/ hydrolyzed protein.

Bland diet improvement?/ more small bowel- Try highly digestible

High fiber improvement/ more large bowel - try high fiber.

Question 14

What should you tell owners in terms of GI diets?

Answer 14

Be prepared, the first one we try may not be the fix all one.

Question 15

What is the pancreas? What is its endocrine and exocrine function? What cells / enzymes are secreted?

Answer 15

 Endocrine function: insulin, glucagon, somatostatin:

 The Endocrine Pancreas (Islets of Langerhans):

• α cells – secrete glucagon – 15-20% of total islet cells
• β cells – secrete insulin and amylin – 65-80% of total islet cells
• δ cells – secrete somatostatin - 3-10% of total islet cells
• PP cells secrete pancreatic polypeptide – 3-5% of total islet cells
• ε cells – secrete ghrelin - < 1% of total islet cells.

 Exocrine function: Digestive enzymes (amylase, lipase, trypsin…)

• Secretion of digestive enzymes
• Secretion of bicarbonate in pancreatic juice
• Secretion of colipase that facilitates the action of pancreatic lipase
• Secretion of intrinsic factor (dog vs. cat) for absorption of cobalamin
• Secretion of bacteriocidal peptide

Question 16

Important image

Answer 16

Question 17

What are some exocrine pancreatic diseases?

Answer 17

EPI- Exocrine pancreatic insufficiency

• pancreatitis

Question 18

Who is most likely to get Exocrine pancreatic insufficiency?

Answer 18

Dogs > Cats

• Breed disposition (German Shepherd, Chow, Collie

Question 19

What causes EPI? What are the signs, diagnostic values, ect?

Answer 19

 May be a result of pancreatitis

 Loss of pancreatic tissue mass

 deficiency in digestive enzymes (lipases, amylase, chymotrypsin, trypsin, etc…)

 Signs: diarrhea, steatorrhea, weight loss, ravenous appetite, coprophagia

 Diagnosis: Low serum TLI

 Many times accompanied by dysbiosis
 Bacteria may use cobalamin and produce folate
 Cobalamin also requires pancreatic intrinsic factor for absorption
 The result- high folate, low cobalamin

Question 20

What is the treatment of exocrine pancreatic insufficiency?

Answer 20

 Treatment: Enzyme supplementation
1 Enzyme preparations
2 Raw fresh pancreas

Question 21

What are nutritional management strategies for EPI?

Answer 21

• Controversial
• Need for high digestibility?
• Fat content?
• Fiber restriction?
• Monitor B12 as needed

Question 22

What commercial diets can be given to patients with EPI?

THIS IS NOT NEEDED TO BE MEMORIZED, JUST AN FYI

Answer 22

Commercial diets:

• Hill’s Prescription Diet i/d
• Purina Veterinary Diet EN
• Royal Canin Digestive Low Fat (dogs)

Home cooked diets:

• May be more digestible
• Need to be complete and balanced

Question 23

What is pancreatitis?

Answer 23

 Inflammation of the acinar tissue of the pancreas

 Involvement of pancreatic enzymes that exacerbate the
inflammation and tissue damage

 Can be acute or chronic

 Variable severity

Question 24

How do you diagnose pancreatitis?

Answer 24

 Diagnosis can be challenging

 Medical history

 Serum pancreatic lipase
immunoreactivity (PLI)

 Abdominal US

 Histopathology

Question 25

What are the risk factors for dogs for pancreatitis?

Answer 25

 Breed

 Diet history

 Obesity

 Drugs

 Toxins

 Pancreatic ischemia, trauma

 Hyperlipidemia

 Hypercalcemia

Question 26

What is the risk factors for cats for pancreatitis?

Answer 26

 Idiopathic ++

 Toxins

 Pancreatic trauma

 Hyperlipidemia

 FIP

 Inflammatory GI and liver disorders (« triad disease »)

Question 27

How can you provide nutritional management of pancreatitis?

Answer 27

 Parenteral nutrition allows to provide the body with energy
without pancreatic stimulation
 When no more vomiting, offer water

 Gradual feeding: increase calories to full RER

 Fat restriction- Dogs < 15% ME fat, < 25% ME fat in cats?
Chronic management/ recovery from acute pancreatitis: Diet history is KEY !!!

causative episode identified (treat, trash), possibility to feed
previous diet, unless chronic pancreatitis has resulted.

Question 28

What does a high folate and low cobalamin suggestive of?

Folate supplementation [in patients with chronic enteropathy]  Small intestinal bacterial overgrowth (SIBO)/ dysbiosis

 Exocrine pancreatic insufficiency

 All of the above may be possible

Answer 28

 All of the above may be possible

Question 29

Is there a benefit to using nutrition to help with dermatological disease?

Answer 29

 The right diets, nutrients, and sometimes nutritional
supplements can have a significant benefit in
improving or resolving certain skin disorders

 Some supplements may include fatty acids and zinc

 High quality/digestibility protein

Question 30

What are some of the adverse food responses?

Answer 30

Food allergens: glycoproteins 10,000-60,000 Da (10-60 kDa)

 Type I hypersensitivity suspected Immediate IgE, mast cell degranulation Types III and IV also possible

 Pathogenesis not well known
 Gut-T cells homing to skin?

 Cutaneous sensitization to food

 Genetic predisposition: IgE production

 Breed: Beagle, boxer, cocker spaniel, WHWT

Question 31

What are the top 3 causes of pruritis?

Answer 31

Flea allergic response

Food allergy

Atopy

Question 32

What is a cutaneous adverse food response?

Answer 32

The most common presentation for a dog or cat with cutaneous adverse food reaction (CAFR) is nonseasonal pruritus, although other syndromes such as otitis externa and gastrointestinal (GI) signs may also be present (indistinguishable from atopy)

Question 33

Can you use food allergy testing to determine what your animal is allergic to? What can be used? what is a food trial?

Answer 33

 While some companies offer “food allergy testing” using serum, saliva, or even hair clippings, the only valid diagnostic test is an elimination diet trial

 Single protein single carbohydrate

 Novel ingredients (diet history!)

 There are a number of veterinary therapeutic diets that can be used for diet trials and long-term management. Home-cooked diets using novel foods are another
option

Question 34

What are potential signs of an adverse food response?

Answer 34

erythema, pruritis, otitis, redness, ear infections ( even chronically) red papules on skin, (thorax and abdomen)

Question 35

What are the most common food sensitivities in dogs?

 Chicken  Beef  Pork  Fish  Turkey

Answer 35

Beef is number one

• followed by chicken in dogs, and fish in cats.

Question 36

What are hydrolyzed protein diets?

Answer 36

 Protein size reduction discourages IgE
crosslinking -> mast cell activation

 Theoretically, protein source irrelevant:
chicken, soy with starch

 Helpful when novel foods fail or have been
already tried

 Why can it fail? Theories
 Hydrolysis not small enough

 Bell distribution of protein sizes

 IgG may be more relevant
 Size of glycoprotein can matter
 Purina HA 11.7 kDa or lower
 Ultamino has 99% of peptides below 6 kDa

Question 37

How long should a diet trial last? If cause reintroduced, how long would it take for allergic signs to show up?

Answer 37

The diet should be fed eight to l0 weeks in dogs and four to six weeks in cats, with no other foods, treats, flavored supplements, bones, etc

 Called Challenge: When the offending food or ingredient is reintroduced to a food-allergic patient, the pet’s signs will flare-up anywhere from immediately to within three days

 Clients often administer medications in cheese, yogurt, or peanut butter and feel the amount given is too small to cause a problem

 Limited-ingredient over-the-counter (OTC) diets are not suitable as elimination diets, as they may contain undeclared proteins
 Cross contamination during petfood production

Question 38

What are other diet related dermatological diseases?

Answer 38

 Zn responsive dermatosis

 Vitamin A deficiency

 Protein malnutrition

 Copper deficiency

 Tyrosine deficiency

Question 39

What is hepacutaneous syndrome?

Answer 39

 Hepatocutaneus syndrome is a rare syndrome that can occur as a result of a glucagonoma, liver disease (vacuolar hepatopathy), and rarely diabetes mellitus or
chronic phenobarbital treatment

 Skin lesions: bilaterally symmetric crusting and ulcerative lesions on mucocutaneous junctions and cutaneous regions where repeated pressure is applied
 footpads, ears, periorbital regions, and limb pressure points

 Often the patients will show hypoaminoacidemia (low plasma amino acid concentrations)

 Glucagon and liver dysfunction lead to a catabolic state which results in amino acid depletion

 Protein is vital for epithelial turn-over, especially in pressure points

Question 40

What is the appearence of a liver of a patient with hepacutaneous syndrome on ultrasound? What is the treatment? What is the prognosis for this syndrome?

Answer 40

 Typical appearance of the liver on ultrasound:
honeycomb liver

 Treatment:
 IV infusion of amino acids (Aminosyn 10% crystalline amino acid solution (100 mL contains 10 g of amino acids) can be given IV, 500 mL/dog, over 8–12 hr

 May need to be repeated as needed until lesions resolve

 High protein, high omega-6 fatty acid diet

 B vitamins and antioxidants is empirically recommended
 Some recommend to add egg yolk as a source of B vitamins, choline
 Prognosis- guarded to poor

Question 41

What are the implications of liver disease?

Answer 41

 The liver gets much of its nutrient supply from the portal vein (rather than from an artery)

 The specific nutrient requirements of dogs and cats with liver disease are currently unknown

Question 42

What is liver disease? What is a common cause for liver disease?

Answer 42

 Liver disease causes altered protein, carbohydrate and fat metabolism

 Vitamin deficiency is common with liver disease
 B vitamin supplementation may assist with energy metabolism

 Vitamin C is produced by the liver and is an important anti-oxidant

 Vitamin E is an antioxidant and can be helpful when there is oxidative damage (for example, copper storage disease)

 Vitamin K is stored in the liver and can rapidly deplete
 Synthesis by bacteria may be reduced due to dysbiosis

Question 43

What is hepatic encephalopathy?

Answer 43

 Hepatic encephalopathy is the term used to describe neurological signs that result from liver dysfunction

 These are typically vague cortical signs: confusion, staring into space, seizures

 Often these occur after a meal

Question 44

What is urate urolithiasis?

Answer 44

 With liver disease, protein metabolism can be affected

 Decreased conversion of uric acid to allantoin

 As a result, uric acid is excreted instead of allantoin

 Uric acid can form crystals and stones

Question 45

What is feline hepatic lipidosis? What cats does it commonly occur in? What is the pathophysiology of the condition?

Answer 45

 Imbalance between peripheral fat stores mobilized to the liver, de novo synthesis of fatty acids and hepatic use of fatty acids
 The fat accumulation overwhelms the hepatocytes and impairs liver function
 Inadequate energy intake can induce hepatic lipidosis in cats

 The degree of energy restriction needed to induce HL was
identified to be between 50% and 75% of the cat’s resting energy requirement
 Commonly occurs in overweight cats that are dysrexic due to concurrent disease
 Peripheral tissue lipolysis is stimulated by catecholamines, adrenaline and noradrenaline during fasting
 Lipolysis is inhabited by insulin

Question 46

What must be done for patients with hepatic lipidosis? What is the ideal plan for refeeding?

Answer 46

 The key to managing feline is to provide nutrition and stop the catabolic process

 In addition, treat underlying disease, correct dehydration, manage hepatic encephalopathy (if present) and infection

 Placing a feeding tube is almost always required in these cases; starting to feed at 25% RER in the first day, increasing gradually as tolerated to full RER
 Dietary protein should not be restricted unless there are signs of hepatic encephalopathy

 Energy is key as it is important to reverse the negative energy balance and stop the catabolic state

 Ideally avoid high fat food; however, energy intake is more important

 Potassium may be decreased due to low intake

 Address refeeding complications if occur

Question 47

What is copper associated hepatopathy?

Answer 47

May be hereditary in certain breeds (Bedlington Terriers,
Labrador)
 Defect in biliary copper excretion

 May also be due to excessive dietary intake of highly bioavailable copper
 Copper form in petfood was previously cupric oxide which has low bioavailability, it was since changed to copper sulfate and copper chelate forms that are more bioavailable

Question 48

What is the diagnosis of copper hepatopathy?

Answer 48

 Diagnosis: Clinical signs indicative of liver disease (jaundice, ascites, HE etc), elevated liver enzymes
 Definitive diagnosis is done with a liver biopsy and
quantification of copper

 Important to differentiate between primary copper
accumulation and secondary copper increase due to chronic
inflammation

Question 49

What is copper storage disease?

Answer 49

Dietary copper reduction/restriction indicated in these cases  May get reduction of copper absorption with long-term
ingestion of increased zinc (unreliable)

 Copper is essential, so must also avoid over-restriction

 Negative clinical consequences of deficiency (i.e. anemia)

Question 50

What are the commercial diets with restrictions of copper? What are the other treatments of copper hepatopathy?

Answer 50

 Only commercially available diets restricted in copper are
therapeutic liver diets (Hill’s l/d, Royal Canin Hepatic)
 Home-cooked diet formulation may be option in these cases

 Avoid high copper foods such as internal organs, seafood, mushrooms etc
 Can be with treatment with chelation, and with zinc
 Zinc induces the synthesis of metallothionine, a protein that binds copper in the enterocytes and renders it unabsorbable (and possibly detoxifies the liver too)

Question 51

What are portosystemic shunts?

Answer 51

 Congenital or acquired vascular abnormalities in the portal vascular system
 Congenital shunts are common in certain breeds including Yorkshire Terriers
 Decreased portal perfusion and decreased liver mass permits encephalogenic material to bypass the
liver

 Protein is typically metabolized to ammonia and then detoxified to urea in the liver, however its possible that heme, RNA and other nitrogenous products also
contribute to clinical signs of hepatic encephalopathy

Question 52

What is the role of protein in liver disease?

Answer 52

 Supports liver regeneration

 Dysfunctional liver (or bypassing in portosystemic shunt)

 increased NH3 -> HE
Protein reduction indicated in cases of hepatic encephalopathy

 but otherwise not desired… unfortunately,
hepatic diets are low protein

 still want to feed as much as tolerated by
individual

Question 53

Besides total amount of protein in HE what else should you be mindful of?

Answer 53

 Not only total amount of protein in HE  but also type & quality

 –some better tolerated…

 –may also reduce incidence of urate
 Avoid:
 Meat based protein, especially liver

 Preferred:
 Vegetable, egg, dairy based proteins

Question 54

What are supplements that are used for patients with liver disease?

Answer 54

• Zinc
   May have antioxidant and hepatoprotective effect independent of dose for reduction of copper absorption
• Carnitine
   Involved in fat metabolism

 Generally not deficient but supplementation may be useful in cases of hepatic lipidosis…

• SAMe
• Milk thistle (sylimarin)

Question 55

What tends to be found in lower quantities in liver diets for both cats and dogs?

Answer 55

 Dog hepatic diets: relatively low protein, low copper, low
purine

 Cat hepatic diets: not available, use renal diets

Question 56

What other options are available for dogs with liver dysfunction?

Answer 56

 Transition to a liver diet is indicated if there is evidence of copper storage, hepatic encephalopathy or urate urolithiasis

 Not every dog with elevated liver enzymes or even liver dysfunction requires diet change!!

 When protein and/or copper reduction not indicated…
 Highly digestible commercial diet +/- supplementation

 Customized complete/balanced home cooked diet