Chapter 8 (pt.1): Other Nutrients (Hill) Flashcards
shock from water in dogs cats
50 in cat 90 in dog ml/kg/hr for 1 hr
puppies and kittens: double adult requirement
water maintenance for dogs and cats
1ml/lb/hr or 50ml/kg/day for dogs and cats
assumes ~ 1/2 ml/lb/hr insensible losses and ~1/2 ml/lb/hr urine production
increases with activity ~ 1ml/kcal is good estimate for all species
rehydration
~2-5 x maintenance for 24-48 hours
minerals
carefully regulated so changes in blood concentration of nutrients are frequently associated with metabolic disease and not nutrient deficiencies.
blood concentrations of nutrients can be normal in the face of severe nutritional depletion
what minerals are deficient in Fl forages
Zn, Cu and Selenium
manganese might be as well but hard to test
are mineral and vitamin supplements necessary in cats and dogs?
no not if they are on a standard commercial diet
incipient
active ingredient
excipient
binders, colorants, palatability enhancer like protein and fat
home cooked diets require supplementation with:
multivitamin/trace minerals
calcium
phosphorus
Ca and P sources
legumes contain adequate Ca
cereal grains and grass hays need Ca supplementation
where can you get Calcium carbonate
limestone
where can you get calcium phosphate
bone meal
where can you get Ca acetate
“phoslo” a very soluble and potent phosphate binder
Ca and P requirements
they are the principle components of ash in guaranteed analysis
Ca: P ratio should be between 1:1 and 2:1
when are abnormalities of blood calcium seen?
Ca and P are well regulated and bone stores are large so the only time you should see abnormalities are associated with disease
Eclampsia
hypocalcemia observed in dogs around parturtiion leading to tetanus, seizures and poor uterine contraction, and prolong QT interval on EKG
tx: 10% Ca gluconate and stop pups from suckling
Calcium deficiency
signs of deficiency are primarily associated with bone resorption (Rickets)
dogs and cats fed all meat diets may receive little Ca and get nutritional hyperparathryoidism and osteoporosis.
lack of natural sunlight and subsequent hypovitaminosis D results in nutritional hyperparathyroidism in REPTILES
P deficiency
hypophosphatemia is primarily observed in starved animals following the reintroduction of food or in diabetics.
signs: low ATP, hi red cell fragility, anemia, hemorrhage and neurological signs
–> insulin causes increased use of P for the phosphorylated intermediates of glycolysis so incipient hypophosphatemia can exacerbate too rapid administrationof glucose or insulin
when are abnormalities of blood Na and K usually seen?
they are well regulated and usually only associated with disease
Salt deficiency
absence of salt in diet can cause: low palatability and appetitie, low growth and low efficiency of feed utilization
signs: hyponatremia includes nausea, inappetence, if rapid in onset can cause osmotic swelling of hte brain and may cause neurologic signs similar to salt poisoning
salt toxicity
salt poisoning (pigs) and hypernatremia and hyperosmolality (dogs) can occur if water is restricted following feeding of high salt diets
signs: neurological. the brain becomes hyperosmotic so that it attracts water by osmosis and swells when drinking resumes
hypokalemia
signs are of irregular cardiac rhythm, flat T waves and in cats muscle weakness, persistent ventroflexion of the neck, increased CPK.
in what animal and condition is hypokalemia common?
in cats with renal failure because of increased renal losses
hyperkalemia
usually secondary to metabolic disease
- ace inhibitors with excess intake
signs: muscle weakness, irregular cardiac rhythm, peaked T waves, prolonged QRS and PR intervals
sulfur sources
sulfur containing amino acids (methionine, cystine, taurine)
vitamins (thiamin, biotin)
sulfur requirements
ruminants require sulfur for protein synthesis when urea is used as nitrogen source. excess contributes to inhibition of Cu absorption
birds use sulfate to synthesize taurine
sheep wool contains substantial amounts of sulfur
sulfur plays a role in large intestinal fermentation
Fe sources
iron filings: <1% absorbed
iron oxide (rust) is used as a red colorant and causes red stool if included in too great an excess
ferrous sulfate and ferrous carbonate (both 10 - 20% absorbable)
haem iron: 30 - 50% available
which minerals compete for absorption sites
Cu, Mn, Zn, Co, Cd
Cu-M, Z, Co, Cd <– sounds funny - a way to remember?
which is more absorable: ferrous (Fe 2+) or ferric (Fe3+)?
ferrous (Fe2+)
what promotes absorption?
reducing agents (like ascorbic acid)
when is absorption increased? decreased?
increased = deficient animals
decreased = replete animals
what inhibits absorption
phytates and vegetable proteins inhibit absorption
like soy protein or fiber
what are some iron containing compounds?
oxygen carriers: hemoglobin and myoglobin
oxidation-reduction enzymes: cytochromes
transport: transferrin
storage: ferritin, hemosiderin
Fe deficiency
signs: microcytic hypochromic anemia, thrombocytosis
primarily due to chronic blood loss (think parasites)
-young kittens exhibit evidence of iron deficiency
hemochromatosis
found in: mynahs, birds of paradise and toucans
signs: mostly seocndary to accumulation of Fe in the liver causing fibrosis, hepatomegaly, ascites, weight loss and dyspnea, hi liver enzymes
tx: symptomatic or phlebotomy
iodine: function
exclusively in thyroid hormones
iodine sources
deficiency is observed where soils are deficient in center of continents away from sea
- seaweed and kelp contain large amounts
- eggs and milk
- cereal and muscle contain a little
iodine content in pet foods
is unknown and possibly of wide variation. this has led to the hypothesis that oscillating exposure to iodine may contribute to the induction of hyperthyroidism in cats
iodine deficiency
- goiter
- deficiency of intake like in seed eating birds
signs: decreased metabolic rate, growth, poor hair coat, decreased reproduction
iodine toxicity
suppresses thyroid acitvity and also causes goiter
Cu sources
most foods but especially legumes and shell fish
Cu sulfate and Cu oxide are added to pet foods
Cu absorption
Zn and Cd compete with Cu in binding of metallothionein
transport in plasma bound to ceruloplasmin
thiomolybdates and phytates inhibit absorption
liver is main storage organ
what inhibits Cu absorption
phytates and thiomolybdates
Cu function:
- hemoglobin synthesis
- melanin formation
- crosslinking collagen and elastin in CT
- formation of tight junctions
- myelin formation
Cu deficiency
may cause dilated cardiomyopathy in cats fed Cu oxide instead of Cu sulfate
signs of Cu deficiency
- microcytic anemia
- ataxia in lambs
- cardiomyopathy
- lack of pigmentation causing grey spectacles around the eyes
Cu toxicity
cattle and sheep exposed to contaminated pastures accumulate Cu in the liver which is rapidly released during stress to produce an acute hemolytic crisis, anemia and hemoglobinuria.
- keep Cu <100ppm
- avoid using non-ruminant blocks for small ruminants because sheep are very sensitive to Cu poisoning
Wilson’s disease or hepatic copper toxicosis: seen in what breed
Bedlington terriers
- genetic defect of Cu metabolism
tx: d-penicillamine which chelates copper and Zn sulfate wwhich competes with Cu for absorption
Zn sources
shell fish, meat, leafy vegetables and whole grains
less available in cereal grains
refined carbs are poor sources
Zn absorption
inhibited by phytates, soybean meal, Ca
competition between Zn and Cu
Zn functions:
metalloenzymes
stabilizing membranes
Zn deficiency in dogs
fed high fiber, high Ca generic dog foods
huskies, malamutes, and rapidly growing dogs until puberty develop hyperkeratotic plaques around mucocutaneous junctions which respond to Zn supplementation
signs of Zn deficiency
- poor apetite, low growth, poor bone, egg shell and feather formation
- poor fertility and small testicles
- parakeratosis
- decreased immune funciton
Zn toxicity
- hemolytic anemia is described in dogs which have swallowed pennies minted after 1983 because they are mostly Zn.
can cause acute pancreatitis
Molybdneum sources
legumes and cereals
liver, kidney and milk
excess Molybdenum and signs of it
interferes with Cu and Su metabolism
signs: anorexia and weight loss, diarrhea and poor reproduction
molbdenum function via metalloenzymes
xanthine oxidase
hydroxylases
Manganese sources
manganese sulfate and oxide
manganese function
mucopolysaccharide synthesis
enzymes pyruvate carboxylase (glycolysis) and superoxide dismutase
manganese deficiency
rare except for chicken
will get perosis or “slipped tendon” when Achilles’ tendons slips off its condyle
low growth, bone malformation, curvature of spine and swollen joints
Selenium sources
soil via plants
hi in meat and fish
AAFCO min should be increased because of low bioavailability
Selenium function
antioxidant in conjunction with vitamin E
Selenium deficiency
lambs, calves and foals: white muscle disease
pigs: liver necrosis, and mulberry heart disease
poultry: exudative diathesis
Selenium toxicity
when > 5ppm
acute: respiratory distress, diarrhea, death
subacute: “blind staggers” - stumbling paralysis, impaired vision, abdominal pain, etc.
chronic: “alkali disease” - low vitality, loss of hair, sloughing of hooves, lameness, etc.
Cobalt metabolism
- essential part of vitamin B12 (cobalamin)
- B12 synthesized from cobalt by intestinal bacteria in ruminants
cobalt deficiency
common on certain pastures in Florida
causes unthriftiness, lacrimation, anemia
Cobalt supplementation
not needed in monogastrics
feed Co containing mineral blocks designed for ruminants
Chromium sources
whole grains, spices, stainless steel
dairy products and veg. sources are low
function of chromium
insulin potentiation
Vanadium function
mimics action of insulin, affects iodine (thyroid) metabolism
