Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
301 Cards in this Set
- Front
- Back
Versus normal conditions, how does the energy requirement of an animal change if the weather becomes hot? Cold?
|
Both will require higher energy requirements. In hot conditions, energy is spent to release heat. In cold conditions, energy is spent to keep warm.
|
|
Generally, how does the total body fat of intact males compare to intact females and why?
|
males generally have a lower body fat composition compared to females because of the effects of testosterone.
|
|
when an animal deteriorates from normal to a low condition score, what tissue types are lost the most?
|
fat and muscle
|
|
what mineral deficiencies can be on the rule-out list for anemia
|
Fe, Cu
|
|
A deficiency of what nutrient causes milk fever, and how is it treated?
|
Hypocalcemia. Treated by injecting intravenously.
|
|
How is RER calculated from body weight?
|
Basal Metabolic rate (kcal) =
70 * body weight (in kg) ^ 0.75 |
|
why is body weight not correlated linearly with basal metabolic rate?
|
BMR is related to body surface area, which ultimately determines oxygen consumption.
|
|
What "type" of energy is estimated in feed for dogs?
|
metabolizable energy (ME)
|
|
What "type" of energy is estimated in feed for cats?
|
metabolizable energy (ME)
|
|
What "type" of energy is estimated in feed for birds?
|
metabolizable energy (ME)
|
|
What "type" of energy is estimated in feed for horses?
|
Digestible energy (DE).
|
|
What "type" of energy is estimated in feed for sheep?
|
Total Digestible Nutrients (TDN)
|
|
What "type" of energy is estimated in feed for beef cattle?
|
Total Digestible Nutrients (TDN)
|
|
What "type" of energy is estimated in feed for dairy cattle?
|
Net Energy Lactation (NEL)
|
|
The bare minimum energy required to sustain an animal that is undergoing absolutely no activity (e.g. comatose)
|
basal metabolic rate
|
|
list the following conditions as rendering the body to require more- or less-than-normal feed intake:
- diarrhea - ileus - fever - pregnancy - estrus - confinement - trauma - lack of liver or gut enzymes |
- diarrhea: more
- ileus (lack of GI movement): less - fever: more - pregnancy: more - estrus: less - confinement: less - trauma: more - lack of liver or gut enzymes: less |
|
What is a Blue Bird label? What nutrients must be listed on it?
|
A standardized feed label, according to AAFCO guidelines, that lists aspects about the contents of a feedstuff, including what type of animal/condition it is made for, nutrient profile, ingredients, manufacturer, etc.
Nutrient profile must list, on a by-weight basis, % protein, % fat, % minerals, % dry matter |
|
how many kcal/gram of energy are contained in
- fat? - CHO? - protein? |
fat: 8.5 kcal/g
CHO: 3.5 kcal/g protein: 3.5 kcal/g |
|
referring to dietary intake, what is Maintenance?
|
no net loss or gain of tissue, regardless of the body condition score
|
|
what is the ballpark estimate on how much water an animal needs per day? How does this differ for babies and obese animals?
|
about 5% of body weight
- babies need more than 5% - obese animals need less because fat requires very little water |
|
Name three major ways in which an animal gets water
|
1. Drinks water
2. water in food 3. metabolic water |
|
what type of energy requirement could be characterized by the energy needed to maintain an animal in a sedentary state, with minimal activity and digestion?
|
resting energy requirement (RER)
|
|
what type of energy requirement could be characterized by the energy needed to maintain an animal that is eating and metabolizing food and has a normal activity level?
|
daily energy requirement (DER)
|
|
how is Daily Energy Requirement (small animals) or Maintenance energy Requirement (large animals) calculated?
|
1.5 - 2 times the RER
RER (kcal) = 70 * weight (kg) ^ 0.75 |
|
name the essential amino acids
|
(Pvt Tim Hall)
- phenylalanine - valine - threonine - typtophan - isoleucine - methionine - histidine - arginine - leucine - lysine (cats need taurine and more arginine) |
|
for equine and hogs, what is the first limiting amino acid when feeding a corn and soybean ration?
|
lysine
|
|
generally, how much food do each of these animals need per day:
- horse (hay)? - beef cow (hay)? - lactating dairy cow (hay)? - sheep (hay)? - dog (dry food)? - cat (dry food)? |
- horse: 15-20 lbs hay/day
- beef cow 20-30 lbs hay/day - lactating dairy cow: 40-60 lbs hay/day - sheep: 2-4 lbs hay/day - dog: 1 cup per 20 lbs body weight - cat: 1/2 cup per day |
|
true or false, production animals are generally considered to be at maintenance? Explain.
|
False
They are usually growing, in gestation, and/or lactating |
|
what are the three basic commercially available small animal diet types and their moisture content and energy density?
|
1. dry - 6-10% moisture; 350 kcal / 8 oz cup
2. semi-moist: 23-40% moisture; 275 kcal / 8 oz cup 3. canned: 68-80% moisture; 350-500 kcal / 15 oz can |
|
what are four common nutritional aspects considered in older small animals?
|
1. lower metabolic rate
2. decreased lean body mass and utilization of protein 3. decreased utilization of vitamins and minerals 4. phosphorus and sodium restriction |
|
which trimester of pregnancy requires the most dietary intake and why?
|
3rd trimester
- fetus is growing exponentially - mammary gland is changing |
|
what are the body condition score targets to give birth to healthy neonates in
- mares? - beef cows? - dairy cows? |
- mare: foaling and breeding at 6/9
- beef cow: calve at 5+/9 - dairy cow: minimize loss to 1 BCS point (out of 5) |
|
what is flushing?
|
increased feeding prior to breeding to increase fecundity
|
|
if a dam is poorly nourished, what typically happens in
- Trimester 1? - Trimester 2? - Trimester 3? |
- Trimester 1: fetal loss
- Trimester 2: the dam is committed to the parasitic fetus, so she will sacrifice her own body tissues. - Trimester 3: glucose and protein disorders in the dam; poor growth of mammary gland (poor production of colostrum/milk); dam will catabolize her own body |
|
what is a typical outcome in the neonate if the dam is deficient in:
- Folate? - Iodine? - Copper? - Selenium? |
- Folate: neural tube defects (e.g. spina bifida)
- Iodine: cretinism - Cu and Se: impaired immune function |
|
what is a common condition in ewes and does as a result of an inappropriate feeding program during gestation?
|
pregnancy toxemia. The dam's stomach is smaller and can not accommodate enough food to support herself and her litter.
|
|
what are negative outcomes in the dam and calf in cows fed poor quality forage during gestation?
|
protein energy malnutrition
- dam may not produce enough colostrum - calves can be skinny and weak |
|
what condition can result in dairy cows that are fed too many cations in their dry ration?
|
milk fever (hypocalcemia)
|
|
why should pregnant mares not be allowed to eat fescue grass in late gestation?
|
it contains a mold (endophyte) that prolongs gestation, resulting in weak foals and no milk
|
|
what is a common complication in pregnant dams that are obese?
|
dystocia (difficult parturition)
|
|
true or false: limiting food intake can
- limit the size of the fetus? - reduce the occurrence of dystocia? |
both are false (common myths)
|
|
how is nutrient intake expected to change as a result of
- sexual activity? - late gestation? - parturition? - post-partum? |
- sexual activity: decreased feed intake
- late gestation: decreased feed intake (stomach is compressed) - parturition: will generally stop eating - post-partum: feed increases until peak lactation (3-6 weeks) |
|
for herbivores, what type of food is optimal for
- gestation? - periparturitient period? - lactation? |
- gestation: high forage
- periparturient: transition ration to acclimate gut to high grain; "lead feed" concentrates 2-3 wk prior to parturition - lactation: high grain |
|
why in camelids and small ruminants is BCS frequently overestimated and what should be done, especially during gestation to prevent a poor BCS score?
|
because their fur can conceal the fact that they are underweight. also, the belly can look deceivingly large when the dam is gravid.
Furry animals should be assessed frequently by palpation to determine BCS. |
|
what is the term for the food designed specifically for reproducing small animals?
|
"growth diet"
|
|
in a diet formulated for reproduction, what nutrients are typically higher with respect to a maintenance diet?
|
protein, fat (carnivores), TDN (ruminants), calcium, phosphorus
(in general, higher energy density) |
|
supplementation of nutrients to the dam to achieve an outcome in the fetus/neonate
|
fetal programming
|
|
in a fetal programming trial supplementing women with DHA, what was the outcome?
|
children with a statistically significantly higher immunity to common illnesses
|
|
what is TPN?
|
total parenteral nutrition. Giving glucose, amino acids, and lipids intravenously.
|
|
the first poop that a neonate takes. What is it called and where does it come from?
|
Called meconium, it is the digesta of amniotic contents.
|
|
what are three metabolic/nutritional needs of the neonate in the 0-24 hour period?
|
- start breathing
- stay warm (brown fat and food) - acquire colostrum |
|
what is an inducible GI enzyme?
|
an enzyme that is upregulated by its substrate. For example, if an animal has low lactase in the GI tract, lactic acid intake in small amounts is required to produce more of this enzyme; otherwise, most of it will pass undigested.
|
|
what are four important things that a neonate must do (physically and physiologically) in the days 1-7 post parturition?
|
1. acquire food frequently
2. rest 3. develop a functional GI system (and supporting metabolism) 4. avoid neonatal pathogens (e.g. diarrhea and ammonia) |
|
how long does it typically take a neonate to start increasing milk consumption, exploring other foods, growing, and increasing its activity?
|
7 days or more
|
|
What are the three "neonatal periods"
|
- day 0
- days 1-7 - day 7+ |
|
which domestic mammals acquire some immunoglobulins transplacentally?
|
puppies and kittens
|
|
what are the three major functional components of colostrum?
|
1. nutrients
2. immunoglobulins (IgG, IgA, IgM) 3. "bioreactive components" (e.g. lactoferritin, lymphocytes) |
|
which major immunoglobulins can be found in colostrum? Where do these Igs end up in the neonate?
|
- IgG - monomeric; absorbed via pinocytosis into the bloodstream
- IgA - dimeric; secretory component; has a local effect in the GI mucosa - IgM - pentameric; has a local effect in the GI mucosa |
|
where is lactoferrin found, and what is its main function?
|
found in colostrum, it helps to prevent microbe growth by sequestering iron from the milk
|
|
compared to milk, what nutrient is in lower concentration in colostrum because of its higher energy density?
|
water
|
|
to obtain adequate antibody transfer, how much colostrum must be consumed by
- puppies? - kittens? - small ruminants? - calves? - foals? |
- puppies: 3-10 mL
- kittens: 3-5 mL - small ruminants: 250-500 mL - calves: 6-8 L - foals: 6-10 L |
|
what procedure is commonly used in FPT horses to provide Ig?
|
blood or plasma transfusion
|
|
what does a colostrometer measure?
|
density of colostrum
|
|
how can passive transfer be assessed?
|
- density of colostrum
neonate serum/plasma assay: - radial immunodiffusion (RID) - refractometry - SNAP tests |
|
what are five common reasons that neonates may not be able to ingest enough colostrum?
|
1. poor udder development ("coke bottle teats")
2. mastitis 3. premature birth 4. poor BCS of dam (maybe) 5. rejection by dam |
|
what specifically causes a toxicosis in mares that causes a thickened placenta, prolonged gestation, and poor/no milk production
|
fescue grass containing endophyte (mold)
|
|
what effect was found in swimmers supplemented with bovine colostrum?
|
"elite" swimmers had lower upper respiratory tract symptoms versus controls. "Regular" swimmers had no difference.
|
|
how is colostrum typically stored, once collected?
|
refrigerated or frozen
|
|
how should colostrum be unfrozen and why?
|
with little heat to prevent denaturing of proteins
|
|
puppies:
- how often should they suckle? - when do they get solid food? - when are they weaned? |
- suckle 4-6 times per day
- solid food at 3-4 weeks (gruel of dam's lactation diet) - wean by 8-10 weeks |
|
foals:
- how often do they nurse? - how often should sick foals be hand fed? - when do they start exploring other food? - when are they weaned? - what should they eat when weaning? |
- nurse 1-2 minutes, 3-7 times per hour
- should be hand-fed minimum 1-2 times per hour - will explore food at several days of age - 4-7 months - feed foal creep feed during weaning (versus mare's ration) |
|
dairy calves:
- when are they separated from dam? - what are they fed? |
- separated at birth
- colostrum day 1, followed by milk replacer |
|
what type of ration allows for better rumen development in the neonate and why?
|
- milk and grain (versus milk and hay) because it has a higher nutrient density
|
|
how does milk total solids compare across species?
|
the species with a higher fecundity tend to produce milk with a higher energy density (thicker and less water) because they must supply nutrients for more young.
|
|
what are four options for orphaned foals to receive milk?
|
1. commercial supplement
2. milk the dam (if foal was rejected) 3. nurse mare 4. raise the foal on a goat |
|
what is the nutritionist's recommended amount of milk to be fed to sick neonates?
|
10% of body weight
|
|
what are four important things to monitor in a sick neonate?
|
1. attitude
2. hydration 3. fecal output and consistency 4. growth rate |
|
what is the main reason proposed in a paper that calorie restriction increases longevity?
|
Our bodies evolved to survive in times of famine, so we are not programmed to handle overabundant food.
|
|
in puppies and kittens, how is the dietary energy requirement (for growth) calculated? How does this change over time?
|
DER = RER x growth factor
the growth factor gets closer to maintenance (1.4-2) as the neonate ages. |
|
for weaned puppies and kittens,
- best method of feeding - frequency of feeding - type of diet |
- rationed; avoid free-choice
- at least 2 feedings per day - small and medium breeds, use growth/lactaion diet - large breeds need food with less energy and less calcium - limit treats and supplements |
|
why is it bad to feed a "urinary tract health" diet to a growing kitten?
|
because these foods can be acidifying and can demineralize bone
|
|
what are seven clinical signs of developmental orthopedic disease?
|
1. contracted tendons
2. wobblers 3. physitis 4. osteochondrosis 5. osteochondritis dissecans 6. angular limb deformities 7. hip displasia |
|
a syndrome of musculoskeletal diseases related to juvenile nutritional deficiencies, and characterized by severe bone deformities.
|
developmental orthopedic disease
|
|
what is developmental orthopedic disease (DOD)?
|
a syndrome of musculoskeletal diseases related to juvenile nutritional deficiencies, and characterized by severe bone deformities.
|
|
what are four risk factors for developmental orthopedic disease?
|
1. genetic predisposition (e.g. large breed dog or excess insulin and IGF-1)
2. overfeeding 3. dogs - excess Ca and Vitamin D 4. Horses - Cu and Zn deficiencies |
|
In ruminants, what is the ultimate nutititional goal for
- harvest animals? - replacement animals? |
- harvest animals: rapid growth; grain early and abundant
- replacement animal: moderate growth; reach targets for puberty |
|
what are two methods to feed market lambs and feedlot heifers/steers?
|
1. high concentrate (> 75%) at weaning and continue until harvest
2. "stocker" phase. Feed high forage for moderate growth and finish on high concentrate rations |
|
for replacement dairy ruminants, why is targeting the weight for puberty important? How does obesity during puberty affect production?
|
because the reproductive systems grow exponentially during puberty. Obesity during puberty is associated with poor mammary development due to deposition of fat in the udder.
|
|
what is stair-step feeding? how does it theoretically work? Pros? Cons?
|
- periods of minimal growth (feeding) interspersed with rapid growth, as opposed to linear feeding based on age.
- Supposedly mimics nature, e.g. limited growth in the winter and rapid growth in the spring - pros: higher milk production - cons: more intensive management; should not be used with horses |
|
for dairy animals, what are the two general considerations for feeding for growth?
|
1. forage availability and quality (pasture and hay)
2. supplementing with concentrates |
|
what are the three basic types of athletic performance and how do they utilize fuel?
|
1. sprint - anerobic glycolysis
2. intermediate (e.g. hunting) - anaerobic and aerobic 3. endurance: aerobic - oxidation of CHO, protein, and fat |
|
why is fat a more efficient way of storing energy than others?
|
because fat does not require water for storage (unlike CHO and protein), it can store more kcal per unit volume
|
|
what are the muscle types, fiber size, contractile speed, glycogenolytic activity, capillary density, and # in endurance animals
|
|
|
what type of muscle fiber is best for endurance athletes and why?
|
Type I because they have a higher capillary density and therefore are efficient at aerobic glycolysis
|
|
what type of muscle fiber is best for sprinters and why?
|
Type III because they have high contractile speed and a high capacity for glycogenolysis
|
|
for performance animals, where do the most water losses occur in the horse, dog, and cow?
|
horse: sweating
dog and cow: respiration |
|
what are the preferred nutrients for the endurance athlete and the sprinting athlete?
|
- endurance: fat
- sprinting: CHO (carb load at least 6 hours prior) |
|
why and how can fat be a useful nutrient for the sprinting athlete?
|
- muscles can be adapted to use fat for fuels, which have more energy density
- takes up to 6 weeks for fat adaptation |
|
how much protein should be supplemented to an athlete's diet?
|
none. The increased intake is adequate to compensate for increased protein demand
|
|
what vitamins are required for horses and dogs for athletic performance?
|
- Horses: A, E, thiamine, folacin, B
- dogs: E, C, B |
|
for athletic performance, what is the role of B vitamins?
|
energy metabolism
|
|
for athletic performance, what is the role of vitamin A?
|
antioxidant
|
|
for athletic performance, what is the role of vitamin E?
|
antioxidant
|
|
for athletic performance, what is the role of vitamin C?
|
antioxidant
|
|
how does DER vary between the different athletic types?
|
- sprinters: close to maintenance
- intermediate: 2.5 X RER - endurance: 5-11 X RER |
|
why would a hunting dog collapse 30-60 minutes into intense exercise if fed immediately prior to hunting?
|
- body has high insulin levels because the dog just ate
- because of this, gluconeogenesis is down-regulated |
|
what is the basic pathogenesis of "Monday Morning Disease" in horses?
|
- grain fed on off-day
- glycogen-loaded muscle rapidly undergoes gluconeogenesis - result is anaerobic respiration and high lactic acid concentrations, leading to quick fatigue |
|
why do you not want to feed forage to a racehorse the night before?
|
because it acts as ballast
|
|
in sprinting horses, what can be supplemented to reduce lactic acidosis?
|
bicarb (if allowed)
|
|
for lactating cows and does, how does net energy requirement, body weight, and net energy lactation change over time?
|
for the first 2.5 months or so, the dam has to produce so much milk that she is in a negative energy balance. she will lose body weight as a result. after that, her intake will exceed requirement and she will gain weight
|
|
for lactating does and cows, why is it important to add grain to the diet?
|
1. their intake is 2-5x maintenance and they have limited intake capacity
2. the udder not sensitive to insulin, so the dam must be able to make abundant CHOs |
|
what is the maximum fat for a ruminant and why?
|
6%, because fat, being a detergent, is bacteriostatic and will disrupt normal flora
|
|
if a ruminant is going to be fed a high grain diet, what should be supplemented along with it and why?
|
Na bicarb to buffer acid production in rumen from increased fermentation
|
|
on a visual observation, how many cows should be chewing their cud?
|
at least 1/2
|
|
how does the distribution of optimal nutrient concentration vary with the degree of performance (e.g. athlete, production, growth, maintenance)?
|
|
|
why do we think that dietary fiber is important for monogastrics?
|
- good stool consistency (constipation vs. diarrhea)
- colonic bacteria convert fiber to butyrate, which nourishes colonic mucosa - soluble fiber will blunt or moderate glucose absorption |
|
name six generalized disorders exacerbated by obesity
|
1. arthritis
2. CV disease 3. diabetes 4. immune function and neoplasia 5. poor reproductive efficiency 6. increased GI and skin disorders |
|
in a recent Canadian study, how did body mass index (BMI) in humans contribute to mortality rates?
|
- severely underweight and severely overweight: higher risk of death
- slightly overweight: lower risk of death versus normal and underweight |
|
what are risk factors for obesity?
|
1. hypothyroidism
2. breed (dog, horse) 3. environment (e.g. too much luch grain for Hereford cattle, who are used to harsh environments) 4. neutering 5. sedentary lifestyle 6. obese owners |
|
in general, how does resting metabolic rate compare in obese versus normal animals?
|
they are the same
|
|
what are the two pathophysiologic types of obesity?
|
1. hypertrophic
2. hyperplastic |
|
why is hyperplastic obesity desirable in beef calves?
|
to increase marbling
|
|
what are the two major ways that the body stores energy?
|
1. glycogen
2. fat |
|
what are the five pro-inflammatory cytokines associated with obesity?
|
CYTOKINES:
1. TNF 2. IL-6 ADIPOKINES: 3. leptin 4. adiponectin 5. resistin |
|
what are the three main sites for fat deposition?
|
1. subQ
2. visceral 3. retroperitoneal |
|
what are the two pathophysiologic types of obesity?
|
1. hypertrophic
2. hyperplastic |
|
why is hyperplastic obesity desirable in beef calves?
|
to increase marbling
|
|
what are the two major ways that the body stores energy?
|
1. glycogen
2. fat |
|
what are the five pro-inflammatory cytokines associated with obesity?
|
CYTOKINES:
1. TNF 2. IL-6 ADIPOKINES: 3. leptin 4. adiponectin 5. resistin |
|
what are the three main sites for fat deposition?
|
1. subQ
2. visceral 3. retroperitoneal |
|
with regards to obesity and treatment of obesity, how are CHO and fat interrelated?
|
- CHO can be converted to fat
- however, fat cannot be converted to CHO - need glucose to burn fat (Krebs cycle) |
|
how do stress and corticosteroids affect lipolysis?
|
they upregulate the process
|
|
how does insulin relate to lipolysis?
|
high insulin inhibits lipolysis and vice-versa
|
|
which body tissues/organs can use NEFAs as fuel?
|
- liver
- muscle - heart - NOT THE BRAIN |
|
when NEFAs enter the liver after lipolysis, what three things can happen to them?
|
1. they can be transported into the mitochondria (via carnitine) and burned as fuel
2. they can be reesterified to trigs and exported by the liver as lipoproteins 3. they can be converted to ketone bodies in the liver mitochondria |
|
which animals are particularly sensitive to hepatic lipidosis and why?
|
cats and ruminants. This because their diets have caused them to evolve to have limited ability to export fat from the liver. They both rely on gluconeogenesis due to their limited CHO absorption/intake.
|
|
what substance is required to transport NEFAs into the mitochondria?
|
carnitine
|
|
what is a common nutritional disorder in horses that could be caused by putting an obese horse onto a rapid weight loss diet?
|
hyperlipidemia
|
|
what is the basic pathophysiological reason why hepatic lipidosis can paradoxically exist?
|
even though the body is in a negative energy balance, the body cannot signal to the liver to release fat. The fatty liver, however, signals to the hypothalamus that it is full, thus decreasing appetite
|
|
what are three risk factors for feline idiopathic hepatic lipidosis?
|
1. obesity
2. stressful event (surgery, new cat, owner on vacation) 3. diabetes |
|
what are six typical clinical signs of feline hepatic lipidosis?
|
1. formerly obese, but now thin
2. anorexia 3. icterus 4. elevated liver enzymes 5. hypoalbuminemia 6. muscle wasting |
|
what is the recommended way to treat a cat with hepatic lipidosis?
|
- assisted feeding through a NG tube, PEG tube, or parenterally
- high quality protein and added fat (high energy density) |
|
what is the Tx and prognosis for a cow in hepatic lipidosis?
|
1. force feed (drench propionate, electrolytes, fluids)
2. IV dextrose 3. B vitamins 4. insulin prognosis: poor |
|
what is the Tx for equine hyperlipidemia? prognosis?
|
- IV fluids + heparin (heparin activates lipoprotein lipase)
- IV dextrose - insulin prognosis: poor |
|
the owner tells you that yesterday, Diogi, his favorite dairy cow, was doing fine, today she is acting a bit strangely, is restless, and not eating. He says Diogi was confirmed to be pregnant by his normal veterinarian, who is on vacation in Poland. He also mentioned that his wife started using a new shampoo and it seems that the cows can smell it when they are being milked. What is a nutritionally based rule-out, what would be the clinical signs, and how would you test?
|
- bovine spontaneous ketosis
- common ketosis: off-feed, firm feces, decreased milk - nervous ketosis: salivation, wandering, blind, hyperaesthetic, circling - check for ketones in urine or milk (urine is better) (the shampoo has nothing to do with anything) |
|
what is the Tx for bovine spontaneous ketosis?
|
- IV dextrose
- oral propylene glycol (glucose precursor converted in rumen) - +/- glucocorticoids |
|
what organ systems should be checked when an early lactation cow is sick?
|
Do the RUMBA.
Rumen Uterus Mammary Gland Bronchial Tree Abomasum |
|
what serious condition can be caused in cows with ketosis?
|
displaced abomasum
|
|
what are six clinical signs for pregnancy toxemia in sheep? prognosis?
|
1. anorexia
2. neurologic signs (e.g. ataxia) 3. constipation 4. hypoglycemia 5. ketosis 6. renal failure prognosis: poor to guarded |
|
pregnancy toxemia in sheep Tx
|
- remove lambs
- IV dextrose - oral propylene glycol - IV fluids - oral calcium |
|
what is the best way to prevent pregnancy toxemia in sheep at high risk of developing it?
|
feed grain in late gestation
|
|
in periparturient queens and bitches, what are two common rule-outs for animals presenting with panting, muscle tremors, tetany, and hyperexcitability?
|
1. eclampsia (hypocalcemia)
2. hypoglycemia |
|
why is hypoglycemia always a rule-out in weak small animal neonates?
|
because they are still developing the systems for glucose regulation; before parturition, the dam regulated the glucose concentration transplacentally
|
|
when an animal stops eating, how long does it take to lose inducible GI enzymes?
|
3-5 days
|
|
what are MCTs and when are they indicated?
|
- medium chain triglycerides
- 6-12 carbons long - not incorporated into chylomicrons - indicated in fat malbosorption syndromes because they are put right into the portal circulation |
|
what is the essential omega-6 FA?
what is the essential omega-3 FA? for each, what are common sources of these nutrients? |
- n-6: linoleic acid (corn and soy oil)
- n-3: alpha-linolenic acid (flax) |
|
what is the process of grain overload?
|
- excess grain consumed
- rapid increase in VFA production - subsequent drop in rumen pH - pH 5, rumen stops - hyperosmolar rumen: dehydration - shift in rumen microbes |
|
what are five clinical signs of grain overload?
|
1. off feed
2. enlarged rumen that sloshes when they walk or is ballotted 3. +/- diarrhea (hyperosmotic rumen) 4. down/dead 5. rumen pH < 5 |
|
grain overload Tx
|
1. IV fluids + bicarb
2. rumen lavage 3. oral antacids 4. parenteral antibiotics 5. hay (no grain) 6 may have to cull |
|
what is low milk fat syndrome? How is it treated?
|
when milk protein exceeds milk fat, usually to a decrease in milk fat.
Treated by adding grain |
|
what are two clinical signs of acute laminits?
|
1. increased digital pulses
2. unwillingness to move |
|
what are two clinical signs of chronic laminits?
|
1. hardship grooves in dorsal wall
2. horse: ventral rotation of the tip of P3 |
|
what other nutrient besides protein is abundant in muscle?
|
phosphorous
|
|
what fractions of nephrons must be destroyed in order to see clinical renal disease?
|
2/3
|
|
renal disease manifests in the excess/deficit of what four classes of blood solutes?
|
1. fluids
2. electrolytes 3. hormones 4. metabolic waste products |
|
what are seven common etiologies for direct kidney damage (besides trauma)?
|
1. toxins
2. infectious disease 3. congenital abnormalities 4. neoplasia 5. immunologic disorders 6. pre-renal disorders 7. post-renal disorders (obstructed urine outflow) |
|
what are four things that can cause pre-renal diesase?
|
1. shock
2. hemorrhage 3. dehydration 4. pregnancy toxemia |
|
what is post-renal disease, and what are three common causes?
|
obstructed urine outflow
1. calculi 2. tumors 3. paralysis |
|
what three major pathological processes are associated with renal damage due to high protein intake?
|
1. increased GFR (because of increased glucagon levels)
2. proteinuria and glomerulosclerosis 3. increased acid load and protein waste products (e.g. uremia) |
|
the presence of excess amounts of urea in the blood, which may be a sign of kidney diesase or failure
|
uremia
|
|
a toxic condition resulting from kidney disease in which there is retention in the bloodstream of nitrogenous waste products normally excreted in the urine
|
azotemia
|
|
clinically, how are the terms uremia and azotemia used differently
|
- uremia is usually applied when speaking of the physiologic state of the animal
- azotemia is usually applied when referring to the results of bloodwork |
|
why do carnivores have a higher protein requirement than herbivores?
|
because carnivores (esp. obligate carnivores such as cats) use protein for gluconeogenesis, whereas herbivores use VFAs
|
|
hardening of the glomerular capillary
|
glomerularsclerosis
|
|
in carnivores with kidney disease, how do we give them enough of their required protein while minimizing further kidney damage caused by protein?
|
give them restricted amounts of high quality (high Essential/Non-Essential) protein (e.g. Hill's k/d diet)
|
|
what is the main clinical pathological result of putting a small animal with renal disease on a diet with restricted, high-quality proteins (e.g. Hill's k/d)
|
decreased BUN
|
|
in human trials, how was reduced protein intake correlated with the progression of renal disease?
|
there was no statistically significant result
|
|
how do omega-3 and omega-6 fatty acids correlate with the progression of renal disease in dogs?
|
omega-3: renoprotective
omega-6: enhanced renal injury |
|
what type of antibody is most related to food allergies?
|
IgE
|
|
what is the molecular weight range of most dietary protein allergens?
|
18-36 kDa
|
|
in dogs, what is the normal site of inflammation in a food hypersensitivity reaction?
|
skin
|
|
what three digestive-related disorders may result in protein hypersensitivity?
|
1. maldigestive disorders such as pancreatitis
2. inflammatory mucosal disorders such as IBD or Crohns 3. T-suppressor dysfunction in GALT |
|
what is the most effective way to treat protein hypersensitivity?
|
use alternate proteins (trial and error)
|
|
what is the difference between food allergy and food intolerance?
|
food allergy involves a bona fide immunologic hypersensitivity, whereas food intolerance results from other factors such as the inability to digest a nutrient (e.g. lactose intolerace) and does not involve an allergic response
|
|
what are three major sources of ammonia in the body?
|
- byproduct of protein breakdown
- conversion of urea to ammonia by urease positive microbes - microbial breakdown of protein |
|
what are four common large animal feeds in which urea supplementation can be beneficial?
|
- corn grain
- corn silage - corn stalks - molasses |
|
if a ruminant has been on a high-forage diet for a long time, why is it dangerous to suddenly supplement the diet with large amounts of urea?
|
because the microbial production of ammonia will exceed the ability of the liver's capacity to convert it back to urea
|
|
what is the classic clinical presentation of an animal with urea/NPN toxicosis?
|
SLUD
- Salivation - Lacrimation - Urination - Diarrhea - ataxia, incoordination, tetany, death |
|
if urea/NPN toxicosis is suspected, what else should be considered as a rule-out?
|
organophosphate toxicosis
|
|
how is urea/NPN toxicosis treated in the ruminant?
|
- acidify the rumen (e.g. with vinegar)
- evacuate the rumen with a tube or surgery |
|
why would ataxia and incoordination be associated with urea/NPN toxicosis in non-ruminants?
|
hepatic encephalopathy
|
|
in NON-ruminants, how can hepatic encephalopathy treated?
|
- restrict protein in diet
- put lactulose in the diet. Microbes ferment this to acid and ion trap ammonia - sterilize the colon (betadine enema) to minimize ammonia formation |
|
what are the two body protein pools?
|
1. somatic: muscle
2. visceral: blood and circulating proteins |
|
what type of protein is catabolized first during a negative energy balance?
|
visceral
|
|
what are four common reasons for protein energy malnutrition?
|
1. inadequate in feed (e.g. poor quality)
2. inadequate intake 3. unable to digest and/or absorb (e.g. Johnes) 4. unable to retain (e.g. renal disease, diarrhea, Johnes) |
|
in humans, protein deficiency despite adequate energy intake
|
Kwashiorkor
|
|
severe protein malnutrition in late gestation females
|
marasmus
|
|
what is "refeeding syndrome?"
|
acute hypophosphatemia associated with rapid provision of CHO to severely malnourished patients. Can lead to electrolyte imbalances, cardiac failure, edema, and death
|
|
in emaciated horses, divided into three cohorts and fed either alfalfa hay, oat hay, or 50% oat hay:50% commercial supplement, what was the result?
|
"refeeding syndrome" was most acute with the highest quality ration (alfalfa), whereas in the mixed diet, it took longer
|
|
what was supplemented to dogs to decrease aggression and hyperactivity?
|
tryptophan
|
|
what are four common diseases associated with hypocalcemia and the species that they affect?
|
1. milk fever (parturient pariesis) in dairy cows
2. transport tetany in mares 3. hypocalcemia in cows, ewes, does 4. eclampsia in bitches and queens |
|
what are two major reasons for hypocalcemia in the cow's periparturient period?
|
1. Ca goes into colostrum
2. they stop eating |
|
what are two hormones to counteract hypocalcemia
|
1. PTH
2. Vitamin D |
|
what is the traditional theory of why cows can't mobilize calcium, thus being predisposed to milk fever? What is the current theory?
|
old theory: High Ca in alfalfa hay has a negative feedback on the parathyroid glands
new theory: alfalfa hay is high in K+, making the cow systemically alkalotic, and the PTH receptors work best at lower pH |
|
what are the clinical signs of early, mid, and late stages of milk fever?
|
- early: mild excitement, tetany, hyperthemia
- mid: depression, flaccid paralysis, recumbency, tachycardia, hypothermia - late: coma and death |
|
what are the three general roles of calcium with regards to muscle tonus?
|
1. in the muscle cells for contraction
2. nerve impulse conduction 3. released by the motor neurons to stimulate muscle contraction (motor unit) |
|
how does muscle tone differ in cows, mares, and bitches during periparturient hypocalcemia?
|
- cows rapidly go to a flaccid state
- horse (transport tetany) and bitches (eclampsia) remain tetanic |
|
how does age affect periparturient hypocalcemia in the cow and the bitch?
|
- cow: older females
- bitch: younger females |
|
how is a cow with milk fever treated?
|
- if down, IV Ca (Ca borogluconate)
- if standing, oral Ca |
|
what responses would be expected from a cow with milk fever after she has been administered calcium?
|
- reduced heart rate
- muscle tonus - defecation and urination - belching |
|
what are three nutritional ways to reduce the risk of milk fever?
|
1. maintain adequate intake in late gestation / early lactation
2. low K diets in dry period (no alfalfa) 3. anionic (acidic) diets in the dry period (boosts PTH receptor affinity) |
|
when does eclampsia occur in the bitch?
|
at peak lactation (3-4 weeks)
|
|
what are five clinical signs of eclampsia in the bitch?
|
1. restlessness
2. vocal (whiny) 3. stiff gait 4. ataxic 5. clonic-tonic seizures |
|
what is a clonic-tonic seizure?
|
cycles of tetany and convulsive spasms
|
|
what are three risk factors for eclampsia in the bitch?
|
1. litter size
2. toy breeds 3. dam is < 4 years old |
|
how is eclampsia treated in the bitch?
|
- IV Ca gluconate
- remove pups for 24 h - wean pups if eclampsia reoccurs - evaluate if Ca > P |
|
when does eclampsia occur in queens?
|
last three weeks of pregnancy
|
|
what are five clinical signs of eclampsia in the queen?
|
1. depression
2. weakness 3. muscle tremors 4. hypothermia 5. flaccidity |
|
what are two risk factors for eclampsia in the queen?
|
1. poor diet
2. excess Ca supplementation during pregnancy (down regulates PTH secretion) |
|
what usually occurs with eclampsia in the queen?
|
hypoglycemia
|
|
how is hypocalcemia (eclampsia) treated in the queen?
|
- IV Ca (1-1.5 mg/kg)
- IV dextrose - oral Ca suspension |
|
what animals are particularly susceptible to nutritional secondary hyperparathyroidism?
|
young, growing animals and reptiles
|
|
why can feeding a meat-only diet cause secondary hyperparathyroidism?
|
because meat has a huge reverse Ca:P ratio
|
|
what are three nutritional causes of secondary hyperparathyroidism?
|
1. "meat-only" diet (too much P)
2. hypovitaminosis D 3. inadequate dietary calcium |
|
why are camelids in Oregon susceptible to secondary hyperparathyroidism
|
because they do not get enough sunshine (versus the Andes, for example) to make enough vitamin D
|
|
what is the end-result of hyperphosphatemia? What is the pathogenesis?
|
- bone degeneration
- hyperphosphatemia --> increased PTH secretion --> increased bone reabsorption |
|
what are the main clinical signs of hyperphosphatemia?
|
- pathologic fractures
- lameness - paralysis (if spinal cord fractures) |
|
what disease in large animals is associated with hyperphosphatemia?
|
fibrous osteodystrophy
|
|
what is grass tetany? clinical signs? what are the two main causes?
|
- hypomagnesemia seen in ruminants
- belligerent, ataxic, muscle tremors, salivation, bruxism (teeth grinding), seizures, recumbency 1. lactating cow on lush spring grass 2. 2-4 month-old calves on milk replacer |
|
how can you tell grass tetany from urea toxicosis?
|
hypomagnesemia is sporadic, whereas urea toxicosis would affect all animals eating the contaminated feed
|
|
what are risk factors for hypomagnesemia in cows?
|
- high dietary concentration of K, N, citrate, and Al, which all decrease Mg absorption
|
|
why can excess dietary potassium (e.g. in alfalfa grass) lead to grass tetany?
|
K reduces Mg absorption in the rumen, thus leading to hypomagnesemia
|
|
how is hypomagnesemia in ruminants treated?
|
- IV, oral, or enema Mg
- high Mg mineral free choice |
|
in small animals, when are magnesium levels usually assessed most often?
|
critical care cases:
- cardiac function - long-term parenteral nutrition |
|
what are the main causes of hypokalemia in cats?
|
- chronic overacidification of the diet (e.g. urinary tract diet)
- anorexia, diuresis, diabetes, insulin therapy, vomiting, diarrhea |
|
what are the clinical signs and treatment of hypokalemia in cats?
|
- ventroflexion of the neck, stiff gait, exercise reluctance
- treatment: IV or oral K |
|
what are two common risk factors for hypokalemia in cows?
|
- off feed (they should be supplemented with K)
- repeated use of corticosteroids |
|
stones in the urinary tract
|
urolithiasis
|
|
what crystals occur with acidic and basic urine?
|
- acidic: struvite
- basic: ammonium urate; Ca oxalate |
|
what is a nidus with regards to urolithiasis?
|
a place for a stone to seed in the urinary tract:
- debris from UTI - mucosal debris (e.g. from inadequate vitamin A) |
|
what are five clinical signs/ways that urolithiasis can be diagnosed?
|
1. aberrant urination (esp. with blood)
2. difficulty urinating or no urination 3. palpation of bladder 4. radiograph/ultrasound 5. crystals in urine and urine pH |
|
what are the two main ways to treat urolithiasis
|
- pH altering diet
- Sx |
|
what is the best way to prevent urolithiasis and what are three ways to do it?
|
- increase water intake
1. add salt to diet 2. feed canned food 3. clean water trough (palatibility) |
|
what three compounds are commonly added to diets to acidify the urine?
|
1. ammonium chloride
2. ammonium sulfate 3. dl-methionine |
|
what areas of the US are deficient and rich in selenium?
|
- deficient - west, mid-west, east coast
- rich: plains, south, south-west |
|
who are at highest risk of selenium deficiency?
|
young animals
|
|
what are two essential functions of selenium-containing proteins?
|
1. GSH --> GSSG (glutathine peroxidase) - antioxidant
2. T4 --> T3 (iodothyronine deiodinase) |
|
what are some syndromes associated with selenium deficiency in ruminants?
|
- white muscle disease
- retained placenta - stillbirths - neonatal weakness - diarrhea - poor doers |
|
white muscle disease:
- etiology - pathogenesis - gross pathology |
- selenium deficiency in ruminants
- due to lack of antioxidant activity, heart muscle is damaged and replaced with fibrous scar tissue, which can mineralize in advanced stages of the disease - heart presents with massive white streaks in the myocardium |
|
what are some syndromes associated with selenium deficiency in horses?
|
- neonatal weakness
- white muscle dz - adult myodeneration - equine degenrative myleoencepalopathy with steatitis |
|
in diseases with selenium deficiency, what nutrient can also be involved?
|
Vitamin E
|
|
what are two common methods to prevent selenium deficiency?
|
1. oral supplementation (e.g. salt block or supplement in grain)
2. parenteral (short term; lasts days to weeks) |
|
why is Se regulated by the FDA?
|
Because a crappy paper from 1940 provided shoddy evidence that it is carcinogenic.
|
|
what equine disease is caused by selenium toxicosis? etiology? Clinical signs?
|
- alkali disease
- selenium-containing plants - cracked hooves, loss of hair on tail |
|
in which animals is copper deficiency most common?
|
ruminants
|
|
Cu deficiency can be caused by high concentrations of what other elements?
|
Mo, S, Fe
|
|
what are four enzymes that require copper and their function?
|
1. ceruloplasmin - antioxidant, RBC formation
2. lysyl oxidase - cross-linking of collagen (involved in developmental orthopedic diseases) 3. tyrosinase - hair color 4. cytochrome c oxidase - nervous system |
|
what are three clinical signs associated with copper deficiency?
|
- achromotrichia - lack of hair color due to lack of tyrosinase enzyme
- lameness / osteochondritis dissecans - lack of bone and cartilage formation - enzootic ataxia - poor formation of spinal cord |
|
what are two ways to treat copper deficiency?
|
1. parenteral injections
2. add (more) copper to mineral supplement |
|
what are two ways to prevent copper deficiency?
|
1. Cu oxide boluses
2. add more Cu to mineral supplement |
|
which herbivore needs the most copper? Least?
|
horses need the most; sheep need the least; cows are in the middle
|
|
what are two pathogeneses for copper toxicosis?
|
1. liver capacity to store copper is exceeded
2. stress-associated Cu release from the liver |
|
who (species, breeds) are particularly susceptible to copper toxicosis
|
1. sheep
2. Bedlington Terriers 3. Doberman pinschers (chronic active hepatitis) |
|
what are 10 clinical and pathological signs of Cu toxicosis?
|
1. anorexia
2. weakness 3. hemoglobinurea 4. hemoglobinemia 5. icterus 6. anemia 7. hemolytic crisis 8. death 9. "gun metal blue" kidneys 10. dark blue urine |
|
is copper toxicosis treated in
- Bedlington terriers? - sheep? |
- Bedlington terriers: D penicillamine (chelates Cu)
- sheep: oral ammonium molybdate and Na sulfate; add moly ration to water |
|
what is phytic acid?
|
a source of phosphorus in forage
|
|
what four minerals can interfere with zinc?
|
Cu, Ca, P (phytic acid in forage), and Fe
|
|
what are three important roles for zinc?
|
1. metalloenzymes, e.g. Cu-Zn SOD
2. hormone formation: testosterone 3. Vitamin A metabolism |
|
Analogy:
Se is to Vitamin E as Zn is to ____ |
Vitamin A
|
|
what nutrient is required for vitamin A metabolism?
|
Zinc
|
|
what are four clinical signs of zinc deficiency in ruminants?
|
1. reduced growth/intake
2. parakeratosis/hyperkeratosis (too much stratum corneum) 3. reduced immunity 4. bad feet |
|
what are four clinical signs of zinc deficiency in horses?
|
1. DOD
2. bad skin 3. immunodeficiency 4. bad feet |
|
what are three clinical signs of zinc deficiency in dogs?
|
1. skin lesions
2. keratitis 3. conjunctivitis |
|
what are two basic ways to prevent zinc deficiency?
|
1. adequate zinc in the diet
2. avoid antagonists |
|
where in the US is iodine deficiency most prevalent?
|
great lakes regions
|
|
what are three clinical signs of iodine deficiency?
|
1. goiter
2. weak, hairless newborns 3. reproductive problems |
|
how is iodine deficiency treated?
|
iodized salt
|
|
what two species are most sensitive to cobalt deficiency?
|
sheep and cattle
|
|
in monogastrics, what vitamin deficiency can occur as a result of a vegan diet?
|
Vitamin B12
|
|
what is the role of vitamin B12 in ruminants?
|
propionic acid metabolism
|
|
what is commonly injected into anorexic animals as an appetite stimulant?
|
B12
|
|
what causes pernicious anemia?
|
hypovitaminosis B12
|
|
why is milk a poor source of iron?
|
lactoferrin sequesters the iron to prevent bacterial growth
|
|
why are baby pigs at risk for iron deficiency?
|
- no dirt or dirty treats to eat
- rapid growth |
|
what are three clinical signs of iron deficiency in piglets?
|
1. anemia
2. dyspnea/thumps 3. poor doer |
|
iron deficiency in piglets Tx
|
- at 7-10 days, inject chelated iron and repeat in 2-3 weeks
|
|
why is IV Fe dextran not the best idea to supplement to race horses?
|
every now and then, it will kill one
|
|
what are the four requirements for a substance to be classified as a vitamin?
|
1. micronutrient
2. essential for metabolism with a defined function 3. specific syndrome noted with deficiency 4. must be supplied in the diet |
|
what is a specific syndrome noted with vitamin A deficiency?
|
night blindness
|
|
what are some provitamins of
- A? - D? - K? |
- A: beta-cartene
- D: ergocalciferol; cholecalciferol - K: menandione (synthetic K3), phylloquinone (K1), menaquinone (K2) |
|
which vitamins
- are involved in energy transfer? - are antioxidants? - are hormones? - are involved in blood clotting? |
- are involved in energy transfer: B vitamins
- are antioxidants: beta-carotene, retinol, tocopherol, C - are hormones: A and D - are involved in blood clotting: K |
|
why are vitamins A and D routinely given to pregnant cows and calves?
|
- to overwinter
- stored or poor forages have little A - no sunshine in barn (D) |
|
why is it inadvisable to give animals grazing on lush pasture vitamins A and D?
|
they are abundant in pasture
|
|
which form of vitamin E is added to diets? which is commonly found in natural sources?
|
- supplement: alpha-tocopherol
- natural: gamma-tocopherol |
|
why is vitamin E supplemented to beef cattle?
|
the meat stays red on the shelf longer (antioxidant)
|
|
how are vitamins and rat poisons related?
|
- warfarin is a Vitamin K agonist
- vitamin D is a rat poison |
|
why should vitamin K3 not be administered?
|
it is a renal toxicant
|
|
what vitamin can be administered to counteract the effect of warfarin toxicosis
|
vitamin K1
|
|
why does vitamin K administration not work on nose-bleeders?
|
because it is due to exercise-induced pulmonary hemorrhage in horses and caudal vena cava rupture in cattle, not a clotting disorder
|
|
what are two signs of vitamin D toxicosis?
|
1. gastric hemorrhage
2. calcification of the great vessels |
|
why did city slickers with TB get healthy at sanatoria?
|
because sunshine-->vitamin D-->better macrophage function
|