Vitamins and Minerals introduction Flashcards
1
Q
is vitamin/mineral nutrition important
A
- critical for the health and growth of animals
- it is important to know what role vitamins and minerals play in animal growth and physiology
2
Q
what are fat soluble vitamins
A
- thiamin (B1)
- riboflavin (B2)
- niacin (B3)
- pantothenate (B5)
- biotin (B7)
- folic acid (B9)
- vit B12 (cobalamin)
- pyridoxine (B6)
- vit c (ascorbate)
3
Q
what are fat soluable vitamins
A
- vitamins A D E K
4
Q
what are common features of mineral nutrition
A
absorption: most microminerals form salt and other compounds which are relatively insoluable ( I and Se are exceptions) - not readily absorbed
transport: minerals often require carrier proteins for transport in the body ( synthesis of these proteins is important in regulation of mineral metabolism)
5
Q
what is chelation
A
- metal ions are reactive is they are chelated they will oxidise
- metals form complexes with a well defined number of organis ligands ( can consist of neutral or anionic chemical groups, proteins and animo acids are common ligands
6
Q
how are minerals stored
A
- have significant storage so deficiency will not occur unless abset from diet from weeks to years (exception Na and K)
- macrominerals (Ca P Mg) stored in bones
- microminerals (Fe Cu Zn Se Cr and others) stored in liver
- often associated with specific storage proteins
7
Q
what are vitamins
A
- organic nutrients required in small quantities for a variety of biochemical functions
- generally, cannot be synthesized by the body and must be supplied in the diet
- vitamin c is synthesised in liver by some animals but not enough
8
Q
what are water soluble vitamins
A
- all B vitamins are absorbed by passive absorbtion at high levels in the gut and by sodium dependent active transport at low levels in the gut
- excesses are excreted in the urine
- toxicity is rarely problem - but possible
- storage is limited (apart from cobalamin B12) and they must be provided regularly
9
Q
what is the difference between monogastrics and ruminants
A
- rumen bacteria can synthesize B vitamins
- monogastrics have some production of B vitamins in the ceca and hindgut but absorbtion in hindgut is limited
10
Q
water soluability vitamines in horses
A
-normal horses can produce most of the B complex vitamins in adequate amounts in its intestinal tract
- young growing foals and horses under stress conditions (sick very hard work and racing) may benefit from B vitamin supplements
11
Q
rabbits and coprophagy
A
- rabbits practice coprophagy, two kinds of fecal matter one hard and one soft
- cosumed directly from the anus
- fermentation in the cecum and the practice of coprophagy provides the necessary aount of most B vitamins
12
Q
what are fat soluable vitamins
A
- non polar hydrophobic molecules
- all are handled by the GI system in the same way as dietary fat
- after absorbtion fat soluable vitamins are transported to the liver in chylomicrons
- in contrast to water-soluable vitamins, fat soluable vitamins can be stored in the body : vitamins A D E K stored in liver , kidney
- vitamin E stored in adipose tissue
- not excreted in urine ; appear in bile and excreted in feces
- because the body can store excess F-S vitamins, toxicity can occur (Vit A D)
- vitamin D is actually not a true vitamin
13
Q
electroyles
A
- maintain osmotic and electrolytic environment in body fluids (maintaining protien function)
- maintain NaK gradient between intracellular and extracellular environment
- transport in nerve and muscel function
- transport of molecules across cell membrane
14
Q
what are electrolyte deficiency symptoms
A
- Na: lethargy, loss of appetite, muscle weakness respiratory depression and areest
- K : elevated blood pressure, muscle weakness, respiratory depression and cardiac arrest
15
Q
what are electrolyte toxicity symptoms
A
Na: dehydration, seizure and coma
K: cardiac arrhythmia and death
16
Q
what are the functions of calcium
A
- bone strength and maintenance
- maintain resting nerve potential
- blood clotting
- serve as 2nd messenger to relay info from outside to inside the cell
17
Q
how does nerve function work
A
- an action potential results in the open voltage gated ca channels resulting in an influx of ca
- this triggers a series of events that results in the synaptic vesicles releasing their neurotrasnmitters
- binding of the neurotransmitter with a receptor in the target cell results in the specific response
18
Q
how does absorption of ca
A
- calcium is absorbed by two distinct mechanism
- active, transcellular absorption = upregulated to increase ca absorbtion when body ca stores are low
- passive, paracellular absorption = occurs all the time and rate is dependent on dietary ca concentration
- and solvent drag dependent on activation of sodium glucose co transporters 1 (SGLT-1) and Na/K ATPase (thus luminal glucose increase Ca absorption)
19
Q
where does passive paracellular absorption of ca occur
A
- in jejunum and ileum
- when dietary calcium levels are moderate and high
- Ca diffuses through tight junctions into the basolateral spaces around enterocytes and into blood
- Up to 50% of absorption in monogastrics
- less important in ruminants because rumen fluid dilutes ca in digesta
20
Q
where does active transcellular absorption of Ca take place
A
- in the duodenum, up regulated when body Ca stores are low
21
Q
what is the three step process of active transcellular absorbtion of Ca
A
- facilitated diffusion of calcium into the enterocyte
- transport across the enterocyte
- active transport into extracellular fluid (ATP to ADP)
- the step where this process is regulated is transport across the enterocyte, which is controlled by the amount of the carrier protein calbindin (vitamin D is dependent Ca binding proteins) present in the cell
- synthesis of calbindin is controlled by Vitamin D
22
Q
what is calbindin
A
- vitamin D induces synthesis of calbindin
23
Q
what is the transcellular absorbtion of Ca
A
- passive and parcellular Ca transport takes place across the tight junctions and is driven by the electrochemical gradient for Ca
- the ative form of vitamin D stimulates the individual steps of transcellular Ca transport by increasing the expression levels of the luminal Ca channels, calbindins and the extrusion systems
- active and transcellular Ca transport is carries out as three step process.
24
Q
what factors affecting Ca absorption
A
- absorption is inhibited by compounds that form insoluable Ca salts
- oxalates, phytates, phopshates form insoluable salts
- undigestible fats for Ca soaps
- a large part of ingested ca is not absorbed and is excreted in feces
25
Q
how is calcium transported in blood
A
- major ca binding factor in blood is gamma carboxyglutamate residues in serum protein (primary;y albumen)
- the production of gamma carboxyglutamate residues on serum proteins is catalyzed by vitamin K
26
Q
how is Ca excretion
A
- excreted by the kidneys - when Ca in serum is high; tightly regulated
- secreted into intestinal lumen when calbindin is downregulated (epithelial cells are sloughed and unabsorbed Ca goes with them)
- sweat (small amount)
27
Q
what is the correlation of ca metabolism and bone
A
- body contains more ca than any other essential mineral
- 99% of Ca in bones and teeth
- skeletal calcium is in the form of hydroxyapatite
28
Q
bone remondeling
A
- bone is constantly being remodeled
- in humans approx. 500mg Ca may enter and leave bones each day
- bone accretion remains constant in animals of a gieven age, decreases with age
- bone reabsorption changes with Ca status and is a major factor in Ca homeostasis
- two types of cells are responsible for removing and depositing Ca and P in bones
- the activity of these cells is under hormonal regulation
29
Q
what is the difference between osteoclasts and osteoblasts
A
- osteoclasts - removes CaP from bone
- osteoblasts - deposit CaP in bone
30
Q
how is Ca and P regulated
A
- the importance of Ca in metabolism means its levels are precisely regulated
- daily variation is rarely more than 3%
- levels are regulated by ( parathyroid hormone, vitamin D and other hormones )
31
Q
parathyroid hormone
A
- released by the parathyroid glands
- parathyroid glands monitor blood Ca in the carotid artery
- secretes PTH when Ca id down
- rapid effects of PTH - increases Ca reabsorption across the renal glomerulus (decreases urinary Ca loss)
- slower effects ( increased rate of intestinal absorption by stimulating production of active form of Vit D
- increase the release of bone Ca stores (recruits osteoclasts )
32
Q
what is the effect of PTH on bone resorption
A
-PTH primary hormone regulating Ca resorption from bone
- PTH increases the numbers of osteoclasts
- this process takes days so is not used for short term regulation of calcium levels
- higher numbers of steoclasrs breaks down more bone and release Ca
33
Q
Vitamin D
A
- not really a vitamin-acts as a hormone (synthesized in the body)
- vitamin D precursors are found in plant and animal tissue
- precursors are converted to vitamin D by sunlight UV on the skin
- works with PTH regulated calcium and P metabolsim
34
Q
effects of Vitamin D on Ca metabolism
A
- increase Ca absorption ( induces expression of calbindin in gut epithelial cells
- increase P absorption
- stimulated sunthesis of collagen and other bone matrix proteins by osteoblasts
- in addition to its role in promoting bone formation stimulates bone resorption by osteoclasts and stimulates osteoclast recruitment
- net effect is higher blood Ca concentrations
35
Q
what other hormones are involved
A
- calcitonin = has the opposite effect of PTH
- estrogen = regulates osteoclast and osteoblast populations
- when estrogen levels low, more bone resorbed; leads to osteoporosis
- supplimental estrogen prevents osteoporosis in postmenopausal women
36
Q
what are the phosphorus-functions
A
- most abundant intracellular anion
- structural: is essential part of mineral portion of bone
- remaining 15-25% of P in solft tissues: component of cell membranes (phospholipids), metabolic ATP,RNA,DNA,NADP
37
Q
how is phosporus absorbed
A
- most absorbed as inorganic form (PO43)
- phosphosugars, phosphoprotein, phosphonucleotides are hydrolyzed to liberate inorganic P
- absorption takes place in small intestine by: passive paracellular diffusion, active trancellular transport
- active trancellular transport is responsive to
production of 1,25 (OH)2-VitD3 is directly stimulated by low blood P
38
Q
P homeostasis
A
- short term regulation of P is not as critical as for Ca
- daily variations as much as 50%
- the same 2 hormones that regulate Ca also regulate P in the body PTH, Vitamin D
39
Q
when P in the blood is low
A
- stimulates 1,25 (OH)2-VitD3 production
- decrease PTH secretion
- increases intestinal absorption of P
- increase serum P
40
Q
when P in the blood is high
A
- increases PTH secretion and decrease 1,25 (OH)2-VitD3 production
- PTH decreases renal resorption of P
- decreases serum P
41
Q
Ca:P inbalances
A
- the regulation of Ca and P works well if the Ca:P ratio in the diet between 1.2:1 to 2:1
- these ratios result in maximal Ca absorption in monogastrics
- excessive dietary P can interfere with Ca absorbtion in the SL
- high dietary P levels leads to large fecal losses and bone reaption
42
Q
ca sources
A
- normally insufficient in plant sources
- normally add meat meal for protein/P, dicalcium phosphate for P and limestone or cacium carbonate to balance Ca:P ratio
- Ca is cheap ; P is expensive
43
Q
calcium suppliments
A
- limestone 35.8% Ca
- calcium Ca rbonate 40%
- oyster shells 38%
44
Q
calcium and phosphorus supplements
A
dicalcium phosphate 23% Ca and 18.2% P
bone meal 29% Ca and 13.6%
45
Q
mg suppliments
A
- dolomite limestone
46
Q
P sources
A
- inorganis = derived from mineral sources , decalcium phosphate
- organis = derived from animal or plant sources
- meat/bone meal-highly digestible
- phytic acid major P source in plants but indigestible by animals
47
Q
phosphoruc mineral supplements
A
- sodium phosphate 32%
- monoammonium phosphate 12% P
- phosphoric acid 23% P
48
Q
Ca vit D P deficiency
A
- similar symptoms for all three nutrients
- difficult to distinguish one another without doing blood chemistry
49
Q
cage layer fatigue
A
- occurs in laying hens at peak production
- due to high requirement for Ca for egg shell formation
- causes bone deformities, fractures and paralysis
- pullets should be fed high Ca to build up reserves and proper Ca P and Vit D levels should be maintained in the diet
50
Q
vitamin D deficiency
A
- rickets and osteoporosis
- potential issue in piglets raised indoors
- limited transfer ascross the placenta, and colostrum is low
51
Q
vitamin D deficieny in humans
A
- very common nutrients deficiency in canada pre WWll
- now we fortify milk vit d
52
Q
P deficiency
A
- rickets in young animals osteoporosis in elderly
- some differences = osteomalacia and poor pigmentation in older animals
- abnormalitites of erythrocytes, leukocytes and platelets
- pica depraved appetite where animals consume dirt, chew on pen materials
53
Q
toxicity
A
- Ca toxicity does not occur normally
- excess ca is simply not absorbed
- P toxicity is rare - usually due to kidnet failure
- Vit D - calcification of soft tissue, avoid megadoses of vitamin D
54
Q
vitamin k
A
- for many years it was beleived that vit k was only involved in blood clotting
- now recognized the vit k is a cofactor in the synthesis of carboxyglutamic acid
- gla resides in responsible for binding Ca in a range of proteins
- upon binding with Ca becomes activated leading to a series of reaction important in the clotting cascades
- deficiency of vit k can reduce bone density
55
Q
poisoning with k antagonists
A
- many of the populatr rodenticides act by inducing a vitamin K deficiency
- warfarin and dicoumarol interfere with recycling of vitamin k and thereby lead to vitamin k deficiency
- a singler feeding on poison bait can kill not only the rodent, but cause bleedin disease in dogs or cats that subsequently ingest them
56
Q
physiologcal effects of vitamin K
A
- gamma carboxylation of glutamic acid residue in proteins
- proteins are = blood coagulation, bone mineralization, cell growth
57
Q
vitamin k and blood clotting
A
- some clotting factors require Ca to bind for activation
- ca only bind after the gamma carboxylation of specific glue residues in these proteins
- these are called vitamin k dependent proteins
58
Q
vitamin k and bone density
A
- vitamin k promotes bone density by the gamma carboxylation of glutamte in the hormone osteocalcin
- vit k deficiency in associated with osteoporosis
59
Q
vit k deficiency
A
- newborn infants have no stores of vit k
- if a supplement is not provided, hemorrhagic disease of newborns can result
- usually given an injection of 1mg vitamin k at birth
- not observed in swine
60
Q
sweet clover poisoning in ruminants
A
- sweet clover contains coumarin
- in spoiled or damaged clover the coumarin is converted to dicoumarin which blocks the vit k cycle
- stiffness, lameness, swellings beneath the skin (hematomas and blood clots) blood in urine or milk
- prevention, sweet clover that is poiled r moldy should not be fed
- treatment = vit k injections or blood transfusions
61
Q
sources of vit k
A
- plants or bacteria
- intestinal synthesis is important; ruminants dont normally require addition vit k
- high levels of feed antibiotics may reduce vit k synthesis
- synthetic source menadione
- synthetic vit k susceptible to oxidation if exposed to sunlight, loisture, choline or trace elements
