Animal Nutrition Test 5 Flashcards

1
Q

How many interactions are known to occur between pairs of minerals (if level of one is increased then digestibility, absorbability, or metabolizability of the other mineral is reduced)?

A

Over 45

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2
Q

How many mineral elements are required in the diet?

A

Good evidence for 20, many nutritionist think there’s more. The text says 22, but the specific 22 minerals can’t be nailed down from the reading)

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3
Q

When a mineral in the body has no function it’s called

A

An innocuous contaminant

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4
Q

Name the macrominerals

A
Mg2+
Na+
P (PO4)
S
Cl-
Ca2+
K+
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5
Q

Name the microminerals

A
Si
Mo
Co
Mn
Zn
Cu
Se
Cr
I
F
Fe
B
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6
Q

Example of mineral involved with hormones

A

Iodine is a part of the thyroxine hormone, which speeds up the body’s metabolism

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7
Q

Calcium constitutes what percent of bone wet weight?

A

9%

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8
Q

What percent of all body calcium is found in the bones and teeth? Soft tissues and blood?

A

99%, 1%

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9
Q

Minerals required for bone lengthening

A

Ca, P, Mg, F

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10
Q

Which vitamin is necessary for calcium transport across biological membranes?

A

D

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11
Q

Optimal dietary Ca:P ratios for nonruminants

A

1:1-2:1

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12
Q

How are fatty acids involved with Ca digestibility?

A

Fatty acids freed from fat digestion bind Ca, forming an indigestible fatty acid-Ca complex (similar to soap). This reduces Ca digestibility

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13
Q

Ca inhibits absorption of what mineral (besides P)?

A

Zn

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14
Q

Chronic Ca deficiency symptoms:

A

Rickets plus acute symptoms. Rickets is a disease of young growing animals which can also be caused by vit D deficiency or P imbalance

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15
Q

Acute Ca deficiency symptoms:

A

Muscle incoordination (wobbly walks), paralysis, even death. “Big head” disease in horses, various bone disorders

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16
Q

2 other names for calcium tetany

A

Milk fever

Parturient paresis

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17
Q

What species is milk tetany common in?

A

Dairy cattle, dogs, sows, and other species

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18
Q

When does milk fever usually occur?

A

Within the first 5 days after parturition (basically bc milk synthesis depletes the blood of calcium)

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19
Q

Problem with calcitonin and milk tetany

A

Female absorbs extra Ca during pregnancy and calcitonin helps deposit it in bones. But when lactation starts after giving birth, BLOOD calcium levels drop bc milk needs the calcium. The resulting low blood calcium stimulates parathyroid hormone production, but this is overridden by the calcitonin that is still present so blood can’t be released from bones, until several hours after the calcitonin was produced when it starts being destroyed. Then when the calcitonin is gone the danger of milk fever is gone, is the female lives that long

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20
Q

Modern and old-days treatment of milk fever

A

Modern: inject Ca, glucose, and Mg. The female will usually recover in less than 30 mins, but another injection may be needed to cure her

Old: reverse milk synthesis mechanism so the milk can be reabsorbed into body. This is done by inflating a cows udder with an air pump and a teat cannula and then sealing the teats with tape

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21
Q

Prevention of milk fever

A
  • feed low calcium diet for 2 weeks before birth to stimulate parathyroid hormone, which will destroy calcitonin
  • inject a big dose of vit D within 7 days prior to birth to stimulate extra ca absorption and therefore increase blood calcium levels (caution: if vit D is injected too soon then vit D toxicity, characterized by soft tissue and joint calcification, and milk fever may result)
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22
Q

What is the most versatile element found in livestock? Why?

A

P, it’s involved in almost every aspect of metabolism

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23
Q

What percent of all body P is found in the bones and teeth? Soft tissues and blood?

A

80%, 20%

Nearly all cells have P in them

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24
Q

Metabolic functions of P

A
  • P combines with Ca to form crystals that resemble hydroxyapatite crystals, and these are components of hard tissues (therefore it’s indirectly controlled by same hormones as Ca bc it “follows” Ca)
  • component of many enzymes (phosphoproteins)
  • energy utilization (ATP for example)
  • buffer in blood
  • protein synthesis (P in RNA and DNA)
  • lipid transport and metabolism and cell membrane structure (phospholipids)
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25
Q

Ca:P ratio in:

Monogastrics
Pigs
Laying hens
Growing chickens

A

Monogastrics: 1:1-1.5:1
Pigs: 1:1-1.2:1
Laying hens: much higher Ca bc egg shell is mostly Ca
Growing chickens: 2:1

Always check the current NRC or Extension Service recommendations

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26
Q

How much plant P is unavailable? Why?

A

1/2-2/3

Phytic acid in plants binds P and the complex (phytate P) is indigestible to monogastrics, which don’t have phytase to free the P from phytic acid

The phytate P in animal manure is an environmental problem

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27
Q

P deficiency symptoms:

A
  • Rickets in growing animals
  • decreased appetite and anorexia
  • reduced productivity
  • abnormal eating or chewing called pica (chewing on wood and bones, eating soil, and a depraved appetite)
  • long term effects in adults result in lameness and reduced bone strength
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28
Q

Percent of Mg bound in bones?

A

70%

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29
Q

Remember: in terms of largest mineral presence, it goes Ca>P>Mg>others

A

:)

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30
Q

Functions of Mg

A
  • bone development and maintenance
  • needed by enzymes for optimal activity (all enzymes that hydrolyze ATP need it)
  • carb, fat, and protein metabolism (bc of bullet above)
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31
Q

Deficiency symptoms of Mg

A
  • neuromuscular hyperirritability (muscle spasms)
  • skin lesions
  • calcium deposits in arteries, kidneys, and soft tissue (arteriosclerosis?)
  • reduced microbial fermentation in rumen and cecum
  • retracted head in calves
  • anorexia and reduced productivity
  • grass tetany
  • bone abnormalities
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32
Q

4 other names for grass tetany

A

Wheat poisoning
Grass staggers
Lactation tetany
Winter tetany

Low blood Mg levels

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33
Q

Grass tetany typically occurs in:

A

Beef cattle that are grazing lush green pastures, especially when they’re lactating (losing Mg in milk) or those grazing heavily fertilized pastures and those is colder temperatures (shivering depletes Mg)

(The grass is typically adequate in Mg but due to poor Mg absorption, blood, bone, and muscle Mg levels are reduced. The poor absorption can be caused by too much P and protein in the grass, so analyzing the grass for Mg alone won’t give you any advanced warning of grass tetany)

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34
Q

Symptoms of grass tetany

A
Standing alone
Loss of appetite
Easy excitability
Viscousness
Grinding of teeth
Salivation 
Incoordination
Collapse
Convulsions
Coma
Death (usually the first indication that you have grass tetany unless you check your heard 3 or more times a day)
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35
Q

How long after first grass tetany symptoms are observed does death usually occur?

A

6-20 hours

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36
Q

Grass tetany treatment

A

Injection of calculi-Mg solution under the supervision of a vet, only if the animal hasn’t gone into a coma yet

If the animal has been unable to walk for a few hours before the treatment, results aren’t usually favorable. Also relapses after treatment are usually fatal.

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37
Q

Grass tetany prevention

A

Really difficult to prevent in grazing livestock bc of all the variables

1) fertilized supplemented with Mg, works best with sandy soils. Expensive solution
2) give each cow 2 oz/day of MgO mixed into a range cube or with grain. Tastes super bad so it’s hard to get them to eat it
3) limit grazing time or feed hay at night
4) feed lots of grain but it’s expensive and defeats the purpose of grazing
5) can also feed Mg carbonate, MgCl, or MgP. The poorest source of Mg is MgO but it’s cheapest

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38
Q

Mg deficiency may play a role in ______ in humans and animals

A

Osteoporosis

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39
Q

Which 3 minerals work together to maintain the osmotic balance in intracellular and extracellular fluids?

A

Na, Cl, and K

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40
Q

Which 2 minerals cause an animal to exhibit deficiency symptoms the fastest if deficient from the diet? Why is this bad?

A

Na and Cl. This is bad bc very few feeds contain enough salt (except seaweed, fish meal, and whey that hasn’t been desalted)

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41
Q

Is K usually deficient in a normal diet?

A

No, both plant and animal product are usually very high in K. However, supplementation of ruminant animals has been beneficial in recent years (especially after shipping stress)

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42
Q

Where are Na, Cl, and K found in vivo?

A

Na: extracellular fluid (90%)
K: intracellular fluid (90%)
Cl: both inside and outside of cells

The Na:K makes an electrochemical gradient surrounding the cell, which regulates nerve impulses and muscle contractions, so these two things are impaired during deficiency of Na and K

(remember the sodium potassium pump)

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43
Q

GENERAL deficiency symptoms for Na, Cl, and K

A

Anorexia, reduced growth, unthrifty appearance, reduced productivity; and death

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44
Q

3 functions of Na

A

1) acid base regulation (93% of bases in the blood have sodium. Think of bicarbonate!)
2) reduced reproduction
3) osmotic balance (water follows Na into the sweat gland)

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45
Q

Only direct water pumps in vivo are in the:

A

Heart
Intestines (peristaltic motion)
Lymph system

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46
Q

Na deficiency symptoms

A
Reduced growth rate
Reduced feed efficiency
Reduced milk production
Weight loss
Drinking urine and licking the ground in salty areas
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47
Q

3 Cl functions

A

1) acid base regulation (associated with 66% of blood acids)
2) component of gastric juice (HCl and salts)
3) osmotic balance, especially of extracellular fluid

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48
Q

Cl deficiency symptoms

A

Depressed growth rate

Other symptoms are probably masked by Na deficiency symptoms which are very fast and overwhelming

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49
Q

5 K functions

A

1) muscle and nerve functions (heart lesions and irregular heartbeat can happen when deficient in K)
2) osmotic balance
3) acid base maintenance
4) enzyme reactions
5) helps cells absorb AAs and glucose

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50
Q

K deficiency symptoms

A
Abnormal EKGs
Growth depression
Unsteady gait
Muscle weakness 
Depraved appetite (pica) and wool biting in sheep
Emaciation and death
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51
Q

Why is S the odd man out in mineral nutrition?

A

It has unique ties to AAs

It’s not required in inorganic form by the body

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52
Q

S functions through its presence in organic metabolites. What is it used to make?

A
The chondroitin matrix of cartilage
Taurine 
Heparin
Cysteine 
Other organic constituents of the body
Feathers, gizzard lining, and muscles of birds
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53
Q

How does S deficiency affect sheep?

A

Reduced wool growth
Reduced weight gain of sheep and cattle

This can occur when you feed NPN instead of protein without supplementing S! However, these effects are the effect of inadequate microbial nutrition on which the host depends for synthesis of organic metabolites, so they can’t be considered as direct effects of S deficiency

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54
Q

Is S toxicity a major problem? Why or why not?

A

No, the intestinal absorption of inorganic S compounds is low

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55
Q

Fe is needed for proper ____ to occur in cells

A

Metabolism

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56
Q

What percent of body Fe is found in hemoglobin? In myoglobin in muscles and hemoglobin in RBCs combined?

A

Over 50%; 60-80%

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57
Q

What 3 molecules can the iron in hemoglobin bind to?

A

Oxygen, CO, and water

CO2 is carried back from the tissues to the lungs but it’s not attached to the iron directly

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58
Q

Is there enough Fe to meet requirements in most feeds? In milk?

A

Yes, no (especially in sows milk so baby pigs are susceptible to Fe deficiency)

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59
Q

How much hemoglobin can blood alone carry vs blood with hemoglobin?

A

1/2 (causes death by suffocation)

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60
Q

What plays the determining role for the homeostasis of iron metabolism?

A

Absorption (no excretion method!)

The intestinal mucosal cells control the amount of iron entering the animals body

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61
Q

Fe deficiency symptoms

A

Anemia (microcytic, hypochromic)
Diarrhea
Oral and skin lesions (due to tissue anoxia)
Decreased cytochrome activity (only in sever deficiency)
The thumps in baby pigs

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62
Q

Describe the thumps

A

Baby pig has a marginal iron supply when it’s born that lasts for 5-6 days. Sows milk has low iron content (lowest of all livestock species) and rapidly growing piglets are using all of their body iron

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63
Q

The thumps symptoms

A
Pallor of the skin
Labored breathing
Rough hair coat
Poor and reduced growth
Respiratory infections
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64
Q

Treatment of the thumps

A

1) inject soluble Fe solution into piglet before 6 days of age and then 1-2 weeks later depending on the product being raised. This method guarantees the pig will get enough Fe
2) oral dose of Fe with a stomach tube at about 4-6 days
3) Fe supplement coated with something sweet or iron water in pig pen
4) give piglets a chunk of dirt
5) feeding iron chelated to AAs to sow may help, but just feeding Fe won’t

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65
Q

Copper functions

A

Required for:

Fe absorption
synthesis of hemoglobin
bone collagen formation
elastin formation (blood vessels)
nerve transmission
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66
Q

Copper deficiency symptoms

A
Hypochronic anemia
Deformed bones
Ruptured aorta
Incoordination
Paralysis and infertility in cows
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67
Q

Copper (toxicity) imbalance effects

A

Tissue necrosis
Jaundice
Brown liver (due to Cu accumulation)

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68
Q

Cobalt function

A

Contained in vitamin B12, similar to sulfur in Met and Cys, so functions are those listed in B12

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69
Q

Cobalt deficiency symptoms

A

Called “wasting disease”

Listless
Anorexia
Weight loss
Normochromic anemia
Death
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70
Q

Cobalt (toxicity) imbalance effects

A

Thyroid hyperplasia (like goiter but goiter is tied to iodine)
Anorexia
Nausea
Diarrhea

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71
Q

Iodine function

A

Contained in thyroxin hormone

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72
Q

Iodine deficiency symptoms

A

Goiter (enlarged thyroid gland)
Hairless piglets
Premature aging
Lowered basal metabolic rate

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73
Q

Iodine (toxicity) imbalance effects

A

Vasodilation
Skin lesions
Nausea
Hyperthyroidism

2-3 g per 70 Kg of body weight is fatal in humans

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74
Q

Zinc functions

A

Required by several enzymes such as:

Carbonic anhydrase
Phosphatase
Other enzymes

Important in carb and amino acid metabolism

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75
Q

Zinc deficiency symptoms

A
Skin lesions
Anorexia 
Slow growth
Stiff joints
Reduced serum zinc
Impaired taste and dwarfism in humans
Parakeratosis in pigs
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76
Q

Zinc (toxicity) imbalance effects

A
Reduces copper absorption
Dermatitis
Corrosion of the GI tract
Diarrhea
Possibly death
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77
Q

Selenium function

A

Component of gluthathione peroxidase (removes toxic peroxides, interacts with vit E which is an antioxidant so it prevents peroxide formation)

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78
Q

Se deficiency symptoms

A

“White muscle disease”:
Liver necrosis
Atrophy of the pancreas

When deficient simultaneously with vit E, results in muscular dystrophy in calves and lambs

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79
Q

Se toxicity (imbalance) effects

A
Blind staggers and alkali disease in western states
Hair loss from tail in cattle and horses
Hooves slough off
Reproduction failure
Anorexia 
Death

Toxicity symptoms are noted with as little as 9 ppm se in diet

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80
Q

Molybedenum function

A

Component of enzymes like xanthine oxide

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81
Q

Mo deficiency symptoms

A

Anorexia

Poor growth

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82
Q

Mo (toxicity) imbalance effects

A

Diarrhea
Anemia
Stiffness

Treatment: feed Cu above the requirement as Cu reduced Mo toxicity and vice versa

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83
Q

F function

A

Strengthens bone and teeth

Helps prevent dental carries (1 ppm in water)

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84
Q

F deficiency symptoms

A

Weak bone and teeth structure

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85
Q

F (toxicity) imbalance effects

A

Bones and teeth lose normal color and become thickened and soft
Mottled enamel in children

2-5 ppm in water produce toxic results in children
Fluorine is a cumulative process

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86
Q

Chromium function

A

??

Required for body cells to be sensitive to insulin

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87
Q

Chromium deficiency symptoms

A

Impaired glucose tolerance (decreased insulin sensitivity, glucose not absorbed)
Cornea (eye) lesions
Anorexia
Poor growth

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88
Q

Chromium (toxicity) imbalance effects

A

Unknown

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89
Q

Silicon function

A

Calcification of chick bone and connective tissue

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90
Q

Silicon deficiency symptoms

A

Small joints

Growth depression

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91
Q

Silicon (toxicity) imbalance effects

A

Not fully understood.

Silicon in urine may be deposited in kidneys, bladder or urethra to form Calculi (water belly), but other factors besides silicon are involved

92
Q

Sulfur function

A

Component of Met and Cys (S must be provided as these in nonruminant)

93
Q

Sulfur deficiency symptoms

A

AA deficiency in nonruminant

Ruminant: reduced MCO fermentation, poor MCO growth in rumen, anorexia, and reduced productivity

94
Q

S (toxicity) imbalance effects

A

Reduces Mo toxicity

May result in Mo and Cu deficiency

95
Q

Manganese functions

A

Component of enzyme

Needed in collagen synthesis (so bone formation)

96
Q

Mn deficiency symptoms

A
Anorexia 
Reduced productivity 
Delayed sexual maturity 
Poor blood clotting
Weak egg shells and bones
Perosis or slipped tendon in poultry
97
Q

Mn (toxicity) imbalance effects

A

Depressed hemoglobin synthesis due to reduced iron absorption

98
Q

Minerals most likely to be deficient in livestock rations:

A
Macro:
Mg
Na
P
Ca
K (in ruminants)

Basically all macro besides S and Cl! “Magical NaP, Calvin Kline.”

Micro:
Mn (young chicks)
Zn (animals fed high grain rations)
Se (area dependent)
I (area dependent)
Fe (baby pigs)

Basically all micro besides Si, Mo, Co, Cu, Cr, F, and B “Man, zoinks, Selena! I feel…”

99
Q

Is mineral toxicity ever a problem?

A

Yes, in several areas of the US it’s more of a problem than deficiency

100
Q

How do you correct toxicities?

A

Mineral antagonisms
However, often the only solution is to dilute a feed with lots of the mineral with another feed that has little of the mineral

Feed formulation and or mixing errors can cause toxicities and deficiencies

101
Q

5 methods commonly used to provide needed minerals to livestock:

A

1) adding free choice minerals in a self feeder (don’t mix in wrong ratio bc then the animal will have to eat too much to satisfy all mineral requirements! Also if one mineral is too high then toxicity or antagonism could occur)
2) adding free choice mineral salt plus a separate free choice feeder for Ca-P so animals can be more flexible in their consumption. (Some scientists think that animals will only eat what they need)
3) adding free choice salt, free choice Ca-P mix, free choice trace mineral mix. This gives the animal more flexibility especially if just salt is the limiting mineral
4) adding the needed minerals to a protein supplement such as a range cattle cube (cube of cottonseed meals, vitamins, salt, Ca, P, trace mineral cube). However, if the animal needs more of one mineral it has no way to get it without eating more range cube or supplement, which isn’t usually available
5) adding the complete mineral mix to a diet plus offering salt free choice. This allows the animal extra salt if they need it. Beef cattle feedlots and dairies usually use this method

102
Q

Don’t mix minerals and vitamins together (unless chelated) for over _____ days. Why?

A

60-90; the minerals may oxidize or bind vitamins, making them both unavailable to the animal

103
Q

Should you feed unneeded minerals? Why?

A

No, it’s costly and there is a chance of mineral antagonisms occurring

104
Q

Why should you protect the mineral feeder from weather?

A

When rainwater accumulates in it, it will turn to brine and reduce consumption

105
Q

How does a fresh supply of water affect mineral consumption?

A

It increases it

106
Q

Why should aluminum be considered as required?

A

Al accumulates in regenerating bone
Al stimulates enzyme systems involved in succinate metabolism
Al has been reported to be essential in female rat fertility
Metabolic requirement unknown

107
Q

Why should arsenic be considered as required?

A

Supplementation of As to purified diet has been reported to:
Increase growth of chicks
Decrease neonatal mortality in rats and goats
Improve birth weight

108
Q

Why should cadmium be considered as required?

A

Rats fed little Cd show a growth depression when maintained in a metal free environment

109
Q

Why should nickel be considered as required?

A

Dietary requirement reported for chicks

Deficiency reported in pigs, goats, rats, and sheep

110
Q

Why should tin be considered as required?

A

Bc of a single report of a growth response to dietary Sn in rats kept in plastic isolators to prevent environmental contamination

111
Q

Why should vanadium be considered as required?

A

Deficiency impairs reproductive efficiency
Beneficial effects of V on rats, chicks, and others have described tissue uptake and movement of V
V stimulates the rate of glucose transport into rat adipocytes
V ions mimic the effect of insulin on glucose oxidation in rat adipocytes

112
Q

Why should barium be considered as required?

A

May be required for growth of some species

113
Q

Why should barium be considered as required?

A

Might be required for growth of mice and chicks

114
Q

Why should rubidium and cesium be considered as required?

A

May replace some of the vitamin K requirements

115
Q

When did today’s vitamin nomenclature arise?

A

1990 in Journal of Nutrition

116
Q

Who came up with the name “vitamin” and when?

A

Casimir Funk, 1912, vitamine. Vita=life, amine= contains N (he thought they all did). But then the “e” of amine was dropped when he realized that some don’t have N

Last group of nutrients to be discovered and quantified

117
Q

Vitamin facts

A
  • Throughout history, vitamin deficiencies have been a major cause of death in both humans and domesticated animals
  • even though they’re only needed in minute quantities, when they’re missing or deficient productivity declines markedly
118
Q

Are commercial vitamin supplements available? How expensive are they?

A

Yes, they’re inexpensive

119
Q

Define vitamin

A

Any group of a feed constituent essential in small quantities to maintain life but not themselves supplying energy (although some are very involved in intermediary metabolism)

They regulate many body reactions, but don’t become part of the body structure

120
Q

Are vitamins inorganic or organic?

A

Organic! But they’re not carbs, fat, or protein

121
Q

4 fat soluble vitamins:

A

K, A, D, E

122
Q

12 water soluble vitamins

A
Ascorbic acid (vit C)
Thiamin (B1)
Riboflavin (B2)
Niacin (B3)
Pyridoxine (B6)
Cyanocobalamin (B12)
PABA (para-aminobenzoic acid)
Pantothenic acid
Biotin 
Choline
Myoinositol
Folic acid (folacin)

Note: myoinositol and PABA are both made by normal gut microbes in animals and people. Under normal conditions, there isn’t evidence for a dietary requirement. Some nutritionists still refuse to put them on the list of water soluble vitamins

123
Q

Vitamins are added to feed components based on:

A

1) Vitamin activity found in the vitamin source (expressed as International Units, I.U., or US pharmaceutical units, USP, per Kg diet)

So IU/Kg or USP/Kg

These systems take into consideration the vitamins chemical structure (several of the vitamins are available in a variety of molecular structures that vary in vitamin activity) and also the digestibility and absorbability of the vitamin

2) weight (not ideal bc digestibility, absorbability, and activity are variable, but it works if these things are known)

124
Q

What are 3 substances that are usually chemically related to biologically active vitamin forms?

A

Antivitamins, vitamin antagonists, and pseudovitamins

The problem: these don’t have vitamin activity but the body can’t tell that they’re not actual vitamins. In addition, antagonists refuse to be replaced by the proper substances, which can shut down metabolism

125
Q

Chemical composition of fat vs water soluble

A

Fat soluble: made of C,H, and O

Water soluble: CHO and also either N, S, or Co

126
Q

Occurrence of fat vs water soluble vitamins

A

Fat soluble: plants in the precursor form (provitamins)

Water soluble: not in provitamin form (Trp can be convert to niacin but isn’t considered a provitamin)

127
Q

Physiological action of fat vs water soluble vitamins

A

Fat: associated with regulation of structural units including building, maintenance, and physiological action

Water: B vitamins play a variety of very important roles in intermediary metabolism. Energy transfer cannot occur without them

128
Q

Absorption of fat soluble vs water soluble

A

Fat: absorbed along with lipid from the gut
Water: absorbed with water across the small intestine

129
Q

Storage of fat vs water soluble vitamins

A

Fat: can be stored in the fat tissue of the body. The storage increases with the intake and can actually reach toxic levels in the body. It can be extensive enough to allow animals to survive, even flourish, on fat-soluble vitamin deficient diets for a long time (even months) without showing deficiency symptoms

Water: only stored in the body for a very short term use. A 2-4 day storage is as good as it gets. Therefore, a constant dietary source is much more important. B12 is the exception, there’s significant B12 storage

130
Q

Excretion of fat vs water soluble vitamins

A

Fat: excreted in feces
Water: B vitamins are generally excreted via the kidney into urine. B12 is also excreted via bile

131
Q

Synthesis of fat vs water soluble vitamins

A

Fat: A, D, and E aren’t made by microbes and must be supplemented in many rations

Water: rumen microbes can make the water soluble vitamins and vitamin K, so these don’t need supplementation

132
Q

Source of vitamin A

A
  • B-carotene precursor found in green and yellow plants
  • corn 1/8 value of green forage
  • milo devoid
  • fish oil (good source)
  • yellow fat
  • liver (polar bear)

Synthetic costs 2 cents/10^6 IU

133
Q

Animal storage in vit A

A

Substantial reserves may be stored in body fat and liver if diet permits (results in yellow fat)

134
Q

Stability of vit A

A

Destroyed by oxidation (hay curing)

This is why new corn has activity but 1 year old corn doesn’t

135
Q

In vivo functions of vitamin A

A

Vision
Epithelium integrity of eye and respiratory, alimentary, reproductive, and urogenital tract
Bone formation

136
Q

Vit A deficiency symptoms

A
Night blindness or total blindness
Diarrhea due to poor nutrient absorption
Pneumonia 
Bladder stones
Sterility
Fetus absorption
Crooked bones
Bone overgrowth
137
Q

Vit A toxicity symptoms

A

Skin disorder
Hair loss
Fragile bone

138
Q

Vitamin D sources

A

Ergosterol precursor
Found in plants
7-dehydrocholesterol precursor found in animals
Both animal and plant sources require sunlight to be converted to active form
Fish oil and sun cured plants are excellent sources

139
Q

Animal storage of vit D

A

Some in liver

140
Q

Stability of vitamin D

A

Good

141
Q

In vivo functions of vit D

A

Calcium absorption
D2 works in all species except poultry
Poultry require D3

142
Q

Vit D deficiency symptoms

A
Rickets (soft bones) due to poor ca absorption
Weakness
Poor egg production
Anorexia 
Reduced growth
143
Q

Toxicity symptoms of vit D

A

Hypercalcificstion of heart, kidney, and joints

Especially toxic to human infants

144
Q

Vit E sources

A

Germ of cereal grains

Green forage

145
Q

Vit E storage

A

Large amounts can be stored in fat and liver

146
Q

Stability of vit E

A

Low, easily oxidized

147
Q

In vivo functions of vit E

A

Antioxidant, functions with Se to detoxify perioxides

Cell membrane stability

148
Q

Vit E deficiency symptoms

A

Membrane damage
Brain lesions in chicks
Degeneration of testes in rats, so it’s a cure for rat impotence

149
Q

Vit E toxicity symptoms

A

None in most species, nausea in humans

150
Q

Vit K storage

A

Bacterial synthesis in the rumen and large intestine (for all but poultry, nonruminants have to practice coprophagy to get the benefit)

Green leafy materials, liver, fish, eggs

Commercial sources (menadione)

151
Q

Vit k storage

A

Some in liver

152
Q

Stability of vit K

A

Fairly stable.
Actively reduced by dicumerol found in spoiled sweet clover (dicumerol used at rat poison), therefore animals fed spoiled sweet clover need higher vit K intake to offset the dicumerol effect

153
Q

In vivo functions of vit K

A

Required for rapid blood coagulation (needed for prothrombin formation which is necessary for proper clot formation)

154
Q

Vit K deficiency symptoms

A

Hemorrhage
Reduced clotting time
Anemia
Weakness

155
Q

Toxicity symptoms of vit K

A

Relatively nontoxic

156
Q

Thiamin (B1) sources

A

Good sources include bacteria, forages, and other feedstuffs

157
Q

Animal storage of thiamin

A

Low (3-9 days)

158
Q

Thiamin stability

A

Destroyed by moist heat

Raw fish contain thiaminase that lowers thiamin activity and can precipitate deficiency symptoms

159
Q

In vivo functions of thiamin

A

Carb metabolism

160
Q

Thiamin deficiency symptoms

A
Edema
Anorexia
Diarrhea
Weakness
Convulsions 
Brain lesions 
Paralysis
Reduced growth
Polyneritis in poultry
Polioencephalonalacia in cattle
Increased blood lactate and pyruvate levels
161
Q

Toxicity symptoms of thiamin

A

Relatively nontoxic

162
Q

Riboflavin (B2) sources

A
Plants 
Yeast
Milk
Eggs
Liver

Most nonruminant diets contain inadequate amounts so always add to nonruminant diet

163
Q

Stability of Riboflavin

A

Good except destroyed by blue and violet light (riboflavin activity of milk in glass bottles and exposed to sunlight is reduced to 0 in about 8 hours)

164
Q

In vivo functions of riboflavin

A

Component of FAD in electron transport chain
Energy metabolism
Protein metabolism

165
Q

Deficiency symptoms of riboflavin

A

Curled toe paralysis and leg paralysis in chicks
Crooked legs, dermatitis, and reproductive failure in swine
Dermatitis in man
Ruminant deficiency unknown
Anorexia and reduced growth

166
Q

Toxicity symptoms of riboflavin

A

Relatively nontoxic

167
Q

Niacin (B3) sources

A
Leafy materials 
Vasodilation
Distillers products
Cereals are generally a poor source
60 mg tryptophan and 1 mg niacin (expensive though)
168
Q

Animal storage of niacin

A

Poor

169
Q

Stability of niacin

A

Very stable

170
Q

In vivo functions of niacin

A
Hydrogen transport (NAD) in glycolysis
Diarrhea 
Dermatitis
Energy metabolism 
Synthesis
171
Q

Deficiency symptoms of niacin

A
Pellagra in humans
Dementia
Lesions on tongue, lips, and mouth 
Nausea
Black tongue in dogs
Anorexia 
Reduced growth
172
Q

Pyridoxine (B6) sources

A

Cereal grains
Yeast
Bacteria
Legumes

173
Q

Animal storage of pyridoxine

A

Poor

174
Q

Stability of pyridoxine

A

Very stable

175
Q

In vivo functions of pyridoxine

A

Fat, carb, and protein metabolism

Antibody formation

176
Q

Deficiency symptoms of pyridoxine

A

Deficiencies are rare

Anemia
Dermatitis
Staggering gait
Convulsions
Anorexia 
Reduced growth
177
Q

Toxicity of pyridoxine

A

Nontoxic

178
Q

Pantothenic acid sources

A

Soybean meal
Yeast
Bran-rich cereals
Corn and meat are poor sources

179
Q

Animal storage of pantothenic acid

A

Poor

180
Q

Stability of pantothenic acid

A

Fair

181
Q

In vivo functions

A

Fat, carbs, and protein metabolism

Constituent of coenzyme A

182
Q

Pantothenic acid deficiency symptoms

A
Goose stepping in pigs
Dermatitis
Eye matting
Paralysis
Hair loss
Fatty liver
Anorexia
Poor growth
Burning feet syndrome in humans
183
Q

Pantothenic acid toxicity symptoms

A

Nontoxic

184
Q

Biotin sources

A

Synthesized in rumen and intestines

Avidin found in egg white ties up biotin and can result in deficiency in animals fed egg white

185
Q

Animal storage of biotin

A

Poor

186
Q

Stability of biotin

A

Very stable

187
Q

In vivo functions of biotin

A

Fat, carbs, and protein metabolism

Carboxylation reactions

188
Q

Biotin deficiency symptoms

A
Dermatitis
Hair loss
Feather loss
Depression
Foot lesions
Fatty liver in birds
Impaired leg coordination
Paralysis in hindquarters of swine 
Anorexia 
Reduced growth
189
Q

Toxicity symptoms of biotin

A

None

190
Q

Choline sources

A

Animal and plant products

Methionine can serve as a methyl donor

191
Q

Choline storage

A

Poor

192
Q

Choline stability

A

Fair

193
Q

In vivo functions of choline

A
Cell structure (membranes)
Fat metabolism
Methyl donor
194
Q

Choline deficiency symptoms

A

Most likely in poultry

Fatty liver
Growth depression
Perosis in poultry
Anorexia
Reduced growth
195
Q

Choline toxicity symptoms

A

None

196
Q

Folic acid sources

A
Liver
Legumes
Tankage
Yeast
Bacteria
Soybean meal
197
Q

Folic acid storage

A

Poor

198
Q

Folic acid stability

A

Poor

199
Q

Folic acid in vivo functions

A

Carb and protein metabolism

Nucleic acid synthesis

200
Q

Folic acid deficiency symptoms

A
Anemia 
Intestinal upsets
Growth depression
Anorexia
Reduced growth
201
Q

Folic acid toxicity symptoms

A

None

202
Q

Cyanocobalamin (B12) sources

A

Plants devoid
Protozoa and bacterial products are good sources
Liver contains some if animal fed adequate diet
Feces are rich in B12 (cow manure factor)

203
Q

B12 animal storage

A

Poor

204
Q

B12 stability

A

Fair

205
Q

In vivo functions of B12

A

Nucleic acid synthesis
Carb and protein synthesis
Propionic acid metabolism
Maturation of RBCs

206
Q

B12 deficiency symptoms

A

Pernicious anemia
Anorexia
Reduced growth

207
Q

Vitamin C sources

A

Citrus fruits
Green leafy veggies
Tomatoes

208
Q

Vitamin C storage

A

Poor

209
Q

Vitamin C stability

A

Good

210
Q

Vit C in vivo functions

A

Formation and maintenance of intercellular material in some species
Has a role in a various redox reactions in living cells

211
Q

Vit C deficiency symptoms

A

Human, pig, bat, some birds and some fish:
Swollen, bleeding gums
Increased oxidation of vit C which increases the requirement
Loosening of teeth
Weak bones

212
Q

Vit C toxicity symptoms

A

Possibly kidney stones

213
Q

PABA sources

A

Plants are good sources

Liver

214
Q

PABA animal storage

A

Poor

215
Q

PABA stability

A

Good

216
Q

PABA in vivo functions

A

Enhances growth of microbes and chicks

217
Q

PABA deficiency symptoms

A

Very rare in livestock

Poor growth in chicks

218
Q

Inositol sources

A

Plants

219
Q

Inositol storage

A

Poor except in sharks

220
Q

Inositol stability

A

Good

221
Q

Inositol in vivo functions

A

Cures alopecia in mice

222
Q

Inositol deficiency symptoms

A

Very rare in most livestock feeding situations

223
Q

In general, vitamins promote:

A

General health and vigor, and are involved in mechanisms to fight stress and disease in the animal such as antibody synthesis

224
Q

Main vitamins that are deficient in ruminants

A

A and probably D in special circumstances

225
Q

Main vitamins that are deficient in swine

A
Riboflavin
Niacin 
Pantothenic acid
B12
Choline 
A
D
Possibly E
226
Q

Main vitamins that are deficient in poultry

A

All vitamins except:
C
Inositol
PABA

227
Q

Main vitamins that are deficient in horses

A

A
D
E
Thiamin