Nutritional Managmement of Gastrointestinal Disease, Pancreatic Disease, and Dermatological Disease Flashcards
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?
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
What is glutamine? Arginine? Where is fat absorbed and what does it stimulate/ cause?
- 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
What are the clinical signs of pets with GI disease?
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
What is B12 and Folate?
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
What can be the results of adverse reactions to food?
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)
What are potential contributing factors to adverse reactions to food?
Potential contributing factors:
Bacterial enterotoxins
Parastism
Malnutrition
What is IBD? Is IBD a specific disease? What is its characteristics? What must you rule out?
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
What are the possible consequences of chronic enteritis?
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
What is the cause of lymphangiectasia? What is the potential consequences of it? What is the treatment?
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
What are different nutrient strategies utilized for patients with chronic enteropathies?
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
What is the difference between acute and chronic colitis?
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
Is chronic GI signs easily treated?
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
What are some different histories prior to gi incidence and what it will indicate?
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.
What should you tell owners in terms of GI diets?
Be prepared, the first one we try may not be the fix all one.
What is the pancreas? What is its endocrine and exocrine function? What cells / enzymes are secreted?
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
Important image
What are some exocrine pancreatic diseases?
EPI- Exocrine pancreatic insufficiency
- pancreatitis
Who is most likely to get Exocrine pancreatic insufficiency?
Dogs > Cats
- Breed disposition (German Shepherd, Chow, Collie
What causes EPI? What are the signs, diagnostic values, ect?
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
What is the treatment of exocrine pancreatic insufficiency?
Treatment: Enzyme supplementation
1 Enzyme preparations
2 Raw fresh pancreas
What are nutritional management strategies for EPI?
- Controversial
- Need for high digestibility?
- Fat content?
- Fiber restriction?
- Monitor B12 as needed
What commercial diets can be given to patients with EPI?
THIS IS NOT NEEDED TO BE MEMORIZED, JUST AN FYI
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
What is pancreatitis?
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
How do you diagnose pancreatitis?
Diagnosis can be challenging
Medical history
Serum pancreatic lipase
immunoreactivity (PLI)
Abdominal US
Histopathology
What are the risk factors for dogs for pancreatitis?
Breed
Diet history
Obesity
Drugs
Toxins
Pancreatic ischemia, trauma
Hyperlipidemia
Hypercalcemia
What is the risk factors for cats for pancreatitis?
Idiopathic ++
Toxins
Pancreatic trauma
Hyperlipidemia
FIP
Inflammatory GI and liver disorders (« triad disease »)
How can you provide nutritional management of pancreatitis?
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.
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
All of the above may be possible
Is there a benefit to using nutrition to help with dermatological disease?
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
What are some of the adverse food responses?
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
What are the top 3 causes of pruritis?
Flea allergic response
Food allergy
Atopy
What is a cutaneous adverse food response?
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)
Can you use food allergy testing to determine what your animal is allergic to? What can be used? what is a food trial?
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
What are potential signs of an adverse food response?
erythema, pruritis, otitis, redness, ear infections ( even chronically) red papules on skin, (thorax and abdomen)
What are the most common food sensitivities in dogs?
Chicken Beef Pork Fish Turkey
Beef is number one
- followed by chicken in dogs, and fish in cats.
What are hydrolyzed protein diets?
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
How long should a diet trial last? If cause reintroduced, how long would it take for allergic signs to show up?
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
What are other diet related dermatological diseases?
Zn responsive dermatosis
Vitamin A deficiency
Protein malnutrition
Copper deficiency
Tyrosine deficiency
What is hepacutaneous syndrome?
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
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?
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
What are the implications of liver disease?
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
What is liver disease? What is a common cause for liver disease?
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
What is hepatic encephalopathy?
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
What is urate urolithiasis?
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
What is feline hepatic lipidosis? What cats does it commonly occur in? What is the pathophysiology of the condition?
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
What must be done for patients with hepatic lipidosis? What is the ideal plan for refeeding?
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
What is copper associated hepatopathy?
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
What is the diagnosis of copper hepatopathy?
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
What is copper storage disease?
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)
What are the commercial diets with restrictions of copper? What are the other treatments of copper hepatopathy?
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)
What are portosystemic shunts?
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
What is the role of protein in liver disease?
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
Besides total amount of protein in HE what else should you be mindful of?
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
What are supplements that are used for patients with liver disease?
- 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)
What tends to be found in lower quantities in liver diets for both cats and dogs?
Dog hepatic diets: relatively low protein, low copper, low
purine
Cat hepatic diets: not available, use renal diets
What other options are available for dogs with liver dysfunction?
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
