(T3) Lecture 12a - Nutritional disorders and wellness diets 2 Flashcards
What is Feline Lower Urinary Tract Disease (FLUTD) linked to?
Urinary pH!
- pH is either too low or too high; both result in unique crystal formation
- not a single disease, but a syndrome = collection of clinical signs that are non-specific
Clinical signs of FLUTD
- Non-specific; depend on location, size and number of crystals or uroliths
- In some cases: partial or total urethral obstruction (very painful and a medical emergency)
Initial signs:
- frequent urination
- urination at inappropriate places
- hematuria
- sometimes strong odor of ammonia
- painful urination by the cat
What is the veterinary treatment if obstruction occurs with FLUTD?
Medical emergency!
- Fluid replacement therapy
- Flushing out of the urolith
- Relief of bladder distension (cystocentesis)
FLUTD: Struvite vs. Calcium Oxalate Uroliths
High urinary pH: Struvite crystals form
Low urinary pH: Calcium Oxalate crystals form
Why is identification of mineral composition or uroliths important?
Dietary management is directed toward eliminating specific type of urolith or crystalline plug
Nowadays, higher incidence of calcium oxalate FLUTD than struvite FLUTD due to increased use of urine-acidifying diets
What are the conditions for STRUVITE crystal formation?
- High concentration of composite minerals:
- Mg
- P
- Ammonium - Sufficient time in urinary tract to allow crystallization
- Urine pH > 7.0
- Small volumes of concentrated urine
- No relation to urinary tract infections
- usually secondary infections, but not the underlying cause of FLUTD
What are the conditions for calcium oxalate crystal formation?
- Calcium oxalate soluble in alkaline pH
- precipitate in acidified urine - Some cats have mild acidemia
- induced by consumption of acidified diet
- metabolic effect: production of acidified urine, increased serum calcium and urinary calcium excretion
- formation of calcium oxalate crystals
Apart from mineral analysis, what instrument might be handy for diagnosis of calcium oxalate vs struvite crystals?
microscope
Long term dietary management of FLUTD
- Removal or dissolution of urinary crystals
- Prevention of urolith formation; depend on type of urolith
FLUTD - Dietary Management
Struvite Uroliths
- dietary dissolution can take months
- monitor (palpation, radiography)
- feed special diet for 1 month following complete dissolution then switch to maintenance diet to prevent
Maintenance diets for prevention of struvites:
- should produce slightly acidified urine
- moderate in caloric density
- high in digestibility
Dietary ingredients that increase urinary acid excretion
- proteins of animal origin, corn gluten meal, methionine, phosphoric acid
- avoid large amount of cereal grains
For cats not drinking enough water: canned food
- increased urinary volume and lower urine specific gravity (high gravity = concentrated urine)
What nutrients are used for struvite urolith dissolution and prevention? What nutrients are used for calcium oxalate prevention?
Phosphorus, sodium, magnesium
Calcium, phosphorus, sodium, magnesium
Can calcium oxalate uroliths be dissolved?
No. Must be removed by surgical intervention or urohydropropulsion
Dogs and cats with kidney disease have progressive loss of what?
Functioning nephrons
- however, kidney has large capacity to compensate
- clinical signs with 70-85% loss of fxning nephrons
- healthy kidneys have tremendous extra capacity
Potential underlying causes of chronic kidney disease
- Trauma
- Infection
- Immunological disease
- Tumors
- Ischemia
- Exposure to toxins
- Older age
*In most cases underlying cause no longer present = difficult to identify when cat or dog develops renal failure
Why does increased water intake occur with chronic kidney disease?
Filtration capacity of kidneys decrease so needs more water to filter out the “bad”
Clinical signs of chronic kidney disease?
Polydypsia and increased urination
- reduced capacity to concentrate urine
- increased volume of urine
- higher water intake to maintain fluid balance
- azotemia = build up of nitrogenous wastes
- uremia = build up of urea in blood
Clinical signs of uremia (linked to chronic kidney disease)
- decreased appetite or anorexia
- vomiting
- depression
- electrolyte and pH disturbances
- mucosal ulcers
- wt loss
- bone demineralization
- anemia
Dietary management of chronic kidney disease
No cure by diet, but diet may minimize clinical signs and contribute to well-being and longevity.
Diet containing high quality protein that meets but not greatly exceeds maintenance requirements should be fed
- restriction of protein does not halt disease
- cats do not tolerate restricted protein
- protein should only be restricted as needed to control signs for dogs
Food should:
- provide adequate calories from CHO and fat to minimize use of body tissues and dietary protein for energy
- be highly palatable to prevent anorexia; done via pat
- include extra water-soluble vitamins if polyuria leads to excessive loss
- restricted in phosphorus
- include potassium citrate to control metabolic acidosis
- contain fermentable fiber to increase fecal N
- contain omega-3 FA to reduce renal inflammation
- restrict Na if secondary hypertension develops
Why focus on protein quantity and quality for chronic kidney disease?
- want to reduce stress/work on kidney
- switch to low protein diet w/ ideal AA profile
What is the mechanisms behind fermentable fiber increasing fecal N excretion? In the context of chronic kidney disease.
- fermentable fiber is a source of energy for microbes; they also need a source of N
- feeding diet lower in protein, less undigested dietary protein for microbes to access an N source; flux of urea
Why does DOD develop in canines?
- Hip dysplasia
- Nutritional secondary hyperparathyroidism
- Osteochondrosis
Why does DOD develop in horses?
- Angular limb deformities
- Flexural limb deformities
- Physitis
- Subchondral bone cysts
- Cervical vertebral malformation
- Osteochondrosis
Regular growth of bones
- Bones grow by initially forming cartilage template, onto which calcium is deposited to form bone = ossification
- Bone ends grow in 2 places: epiphyseal plate and cartilage
*REMEMBER, CONTROLLED GROWTH AND NOT MAXIMUM GROWTH
What does osteochondrosis cause?
Inadequate blood supply to reach cartilage
- creates thickened cartilage layer
- over time, abnormal cartilage is weakened
- causes inflammation and arthritic changes
What are the 3 primary forms of osteochondrosis in dogs?
- Ununited anconeal process
- Fragmented coronoid process
- Osteochondrosis dissecans
*all types cause arthritic changes if left untreated
Clinical symptoms of osteochondrosis in dogs
- Lameness and pain in affected joint
- Affected animals may try and compensate for lameness by restricting movement of affected joint
Risk factors of DOD in dogs
- multifactorial
- most critical period during growth phase, before epiphyseal closure
- risk factors though to increase risk of osteochondrosis: genetics, management, nutrition
Many dogs with osteochondrosis are what in the litter? What about horses?
The best looking, biggest, and fastest!
- dogs that managed to push out litter mates from feeding bowl, and are growing too fast
In horses, osteochondrosis mainly occurs in foals that are most rapidly growing
- may not be fed diets that are adequately designed to meet predicted nutrient requirements
High energy intake (starch and sugar in horses) directly affects growth velocity via what?
Nutrient supply through changes in concentrations of growth hormone, IGF-I, T3, T4, insulin
Feeding of high-energy foods
- increased risk when highly palatable, energy-dense foods are fed free-choice
- fat content must be considered
- affects growth velocity
- increased hormonal influences enhance mitotic activity of proliferative cartilage cells
- articular cartilage less well supported by solid bone plated in rapidly growing animals
- biomechanical stress induced by rapid weight gain
Feeding of high-calcium foods
- disturbed endochondral ossification, retained cartilaginous cores in distal radius and ulna and delayed skeletal maturation and growth of bone length
- competition of Ca with other minerals or direct stimulation of hormonal effects (PTH or calcitonin) or acid-base balance
- higher blood calcitonin increases deposition of Ca in bones
What could be a danger of feeding calcium supplements to growing horses?
- overfeeding calcium
- just bc you have a fast growing animal, must formulate a diet for that animal (don’t mess around with supplements)
4 preventions of DOD
- Determine if animal is at risk: breed
- If at risk: control nutrients of concern (energy, calcium, phosphorus, feeding time) through food composition and feeding method
- Do not add vitamin or mineral supplements to balanced foods, particularly Ca, P, Vit D and A
- Determine animal’s BCS
DOD - Treatment of Affected Dogs
- Determine nutritional imbalance
- Food should be formulated for large- or giant breed puppies
- Food should be meal-fed
- If a well-balanced growth food was being fed and skeletal disease occur, reduce food intake up to 25%
- No vitamin or mineral supplements should be given to dogs eating balanced food
- Treatment for specific problems: pain relief, exercise restristriction, surgery
What could be the danger of feeding puppies with adult maintenance foods to decrease energy intake?
Growing puppy diet, needing more energy and protein, so decide to switch to a maintenance diet for adults = less energy
- controlled energy but didn’t look at other nutrients = imbalance of vits and minerals
- can’t just look at one component
DOD - Treatment of Affected Horses
- Determine nutritional imbalance
- Food should be formulated for young, growing foals
- Nonfiber CHOs should be meal-fed; forages should be of low quality or fed to meet, but not exceed, energy intake
- If a well-balanced growth food was being fed and skeletal diseases occur, reduce nonfiber CHO intake
- No vitamin or mineral supplements should be given to horses eating balanced food
- Treatment for specific problems: pain relief, allow voluntary exercise
