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GI > Minerals and vitamins > Flashcards

Minerals and vitamins Flashcards

1
Q

Define mineral

A

Inorganic element

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2
Q

Define macro-element

A

Required in large amounts

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3
Q

Define micro-element/trace-element

A

Lower amounts needed

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4
Q

Define bioavailability

A

Ease of extraction from a source

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5
Q

Define pica

A

Eating non-food sources, can be indicative of a depraved appetite

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6
Q

Define vitamin

A

Organic compounds that are required in small quantities for normal growth and maintenance of animal life (can be fat or water soluble)

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7
Q

Define pro-vitamins/vitamin precursors

A

Many vitamins consumed as non-active dietary form which requires chemical change to function as the vitamin

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8
Q

List the essential fat soluble vitamins

A
  • A (retinol)
  • D2 (ergocalciferol)
  • D3 (cholecalciferol)
  • E
  • K (phylloquinone)
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9
Q

List the essential water soluble vitamins

A
  • C (ascorbic acid)
  • B complex (thiamin, riboflavin, nicotinamide, pyridoxine, pantothenic acid, biotin, folic acid, choline, cyanocobalamin)
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10
Q

List the essential macro minerals

A
  • Calcium
  • Phosphorous
  • Magnesium
  • Sodium
  • Potassium
  • Chloride
  • Sulphur
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11
Q

List the essential trace elements

A
  • Iron
  • Zinc
  • Copper
  • Iodene
  • Manganese
  • Molybdenum
  • Cobalt
  • Fluorine
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12
Q

What is deficiency?

A
  • Not having enough of something

- Leads to death

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13
Q

What is toxicity?

A
  • Having too much of something

- Leads to death

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14
Q

Describe bioavailability

A
  • Just becuase something is present does not mean it can be extracted or, in the case of proteins, that it has the correct AA profile
  • Depends on chemical form, other compounds that can interact, age, gender, species, body stored, environmental (organic or inorganic)
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15
Q

Explain the relevance of soil consumption

A
  • Pica/geophagy
  • Ruminants eat grass, ripping action, likely to ingest soil
  • More likely to eat soil in wet weather
  • Also when very windy and dry
  • Likely to have high normal ingestion of soil
  • Soil contains some impotant nutrients
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16
Q

What is the role of sulphur in the body?

A
  • In proteins containing cystine, cysteine and methionine
  • Also in vitamins (biotin and thiamin), hormones (insulin, oxytocin), metabolites (CoA), chondroitin sulphate (cartilage, bone, tendons, blood vessel walls)
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17
Q

Describe the occurence of sulphur deficiency

A
  • Mostly ruminants
  • Sulphur deficiency is also protein deficiency in non-ruminants
  • Feed ruminants non-protein nitrogen sources, divorces sulphur and protein
  • Enough protein but not enough sulphur
  • Wool approx 4% sulphur, woolier more likely to be deficient
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18
Q

What are the effects of sulphur deficiency?

A
  • Decreased fibre quality, eventually shed
  • Decreased rumen function
  • Increased salivation and lacrimation
  • Growth retardation, emaciation and death
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19
Q

Describe sulphur toxicity

A
  • Excess dietary sulphur converted to H2S
  • May cause reduced rumen motility, nervous and respiratory distress
  • Has major role in other mineral interactions (iron and copper, copper and molybdenum, copper and sulphur)
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20
Q

Outline the nutritional needs during pregnancy and lactation

A
  • Aim for ideal BCS before mating
  • Last 3 weeks of pregnancy change diet
  • Do not supplement Ca and vit D
  • Feed small, frequent meals near end of gestation
  • Growth type diet
  • Feed free choice at peak lactation
  • High caloric density, increased protein, inreased calcium
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21
Q

Outline the nutritional needs of senior cats/dogs

A
  • Change to senior type food
  • Higher in fibre,essential fatty acids, zinc and B vitamins
  • Risk factor management for geriatric disease
  • hgih levels of dietary antioxidants
  • Smaller, more frequent meals
  • Alter feeding amount to maintain optimum body conditions
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22
Q

Explain the importance of a carnivorous diet for cats

A
  • Need taurine, arachidonic acid and pre-fromed vit A
  • Only found in animal tissues
  • Insufficient taruine leads to cardiomyopathy adn irreversible blindness
  • Higher pH than 6.2-6.4 risk bladder stones
  • Contrlled lgel of magnesium to help prevent feline lower urinary tract disease
  • Wet ratehr than dry to avoid FLUTD
  • Need pre-formed retinoids in diet, do not utilise carotenoids
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23
Q

Outline rabbit nutrition

A
  • Long fibre essential (dental, behavioural)
  • Protein 13-18% DM
  • High quality protein
  • No added dietary fat required
  • Cits A, D and E required in diet
  • Coprophagy
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24
Q

Outline guinea pig nutrition

A
  • Similar to chinchilla
  • Coprophagy
  • Provide vit C, cannot synthesise it
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25
Q

What is the function of vitamin K?

A

Maintenance of normal levels of blood clotting proteins (II, VII, IX, X, protein C and protein S)

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26
Q

What are the sources of vitamin K?

A
  • Exists naturally as
  • K1 (phylloquinone) in green vegetables
  • K2 (menaquinone) produced by intestinal bacteria
  • Also K3 as synthetic mendione
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27
Q

Briefly describe the forms of vitamin K

A
  • naturally occuring are fat soluble
  • Absorbed from intestine only in presence of bile salts and other lipids through interactions with chylomicrons
  • Synthetic is water soluble, absorbed irresepctive of presents of intestinal lipids and bile
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28
Q

How does vitamin K deficiency occur?

A
  • Fat malabsorptive diseases
  • Long term antibiotic use (stops bacterial production of K2)
  • Intestine of newborns sterile if infant lacking from early diet
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29
Q

How does vitamin K carry out its function?

A
  • Cotting proteins synthesised as inactie precursor proteins
  • Conversion from inactive to active requries post-translationa modification of specific glutamate residues
  • Modification is decarboxylation and enzyme responsible requires vit K as cofactor
  • Reduced hydroquinone form of vit K converted to 2,3-epoxide form
  • Regeneration of hydroquinone form requires uncharacterised reductase
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30
Q

Describe the clinical signs associated with products that interfere with vit K function

A
  • Anticoagulants
  • Warfarin similar shape to vit K
  • Takes vit K’s place in regernation of hydroquinone form using uncharacterised reductase
  • Coumarin toxicity results in coagulopathy and patients present with bleeding tendencies
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31
Q

Describe calcium absorption within the GI tract

A
  • Absorbed passively and actively
  • Controlled by calcitriol, parathyroid hormone and calcitonin
  • Calcitriol and parathyroid hormone increase GI Ca absorption
  • Calcitonin decreases it
  • Absorption increases with increasing calcium concentration in intestine (by diffusion mostly)
  • When requirement for calcium high but Ca of feed is low, increased active transport
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32
Q

How does calcitriol increase calcium absorption?

A
  • Stimulates active transport

- Increases synthesis of calcium-binding transport proteins

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33
Q

Describe the role of calcitriol in calcium regulation

A
  • Increases active transport of Ca from gut to blood
  • Binds to intracellular receptors in cells that transport calcium i.e. the intestine, kidneys, udder and shell gland
  • Also in cells in immune syste,, muscle, endocrine tissue and in bone
  • Required for normal functioning of osteoclasts and osteoblasts
  • 1-hydroxylase enzyme (catalyses production of calcitriol) stimulates by parathyroid hormone
  • Production inhibited by hypercalcemia and hyperphosphatemia
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34
Q

Describe the role of calcitonin in calcium regulation

A
  • Peptide hormone
  • Produced in thyroid gland
  • Hormone acts to reduce concentration of Ca2+ in extracellular fluid by inhibiting bone resorption and increasing urinary excretion of calcium
  • Secretion regulated by concentration of Ca2+ in plasma (not secreted below certain level)
  • Increasing levels within normal range leads to linear increase in secretion
  • Gastrin, secretin and CCK stimulate calcitonin secretion
  • Levels increase after feeding, even when concentration of Ca2+ has not changed
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35
Q

Describe the effect of Ca2+ on parathyroid hormone secretion

A
  • Ca2+ concentration in ECF regulates PTH by direct -ve feedback
  • Receptor coupled to G-protein controls exocytosis of PTH-conaining vesicles by second messengers
  • Continuously secreted at moderate rate when Ca2+ is in normal range
  • Elevated calcitriol in plasma inhibits synthesis and secretion of PTH at given Ca2+ concentration
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36
Q

What is the action of parathyroid hormone in controlling calcium?

A
  • Binding of PTH to membrane receptors increases intracellular concentration of cyclic AMP
  • Affects certain enzymes and transport mechanisms
  • Increases bone resorption and formation of calcitriol in the kidneys
  • Net effect is to increase Ca2+ concentration in ECF
  • Rapid and long term effects
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37
Q

What are the rapid actions of parathyroid hormone in calcium control?

A
  • Stimulates osteoblasts and osteocytes to release Ca2+ from bone
  • Increases reabsorption of Ca2+ by renal tubular cells adn reduces loss of calcium in urine
  • In simple stoamched animals reduces reabsorption of phosphate ions in renal tubules
  • Renal excretion of phasphate increases
  • Prevents rise in plasma phosphate concentration that would be unfavourable for dissolution of bone mineral crystals
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38
Q

What are the long term actions of parathyroid hormone?

A
  • Changes in bone metabolism and intestinal absorption of calcium
  • Mediated via effect of PTH on renal production of calcitriol
  • Increased synthesis of calcitriol in the kidneys
  • In turn increase intestinal absorption of calcium and phosphate
  • Enhanced activity of osteoclasts in bone tissue, both by reruitment of new cells and by increased bone resorption by individual cells
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39
Q

What are the major roles of iron?

A
  • Cytochromes (exploit oxidation and reduction of iron)
  • Lots of iron in oxidative phosphorylation
  • All of TCA cycle enzymes need iron as a cofactor
  • Catalase, peroxidases, phenylalanine hydrolase
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40
Q

Where is iron stored?

A
  • 90% stored combined with proteins
  • Haemoglobin
  • Transferring (iron transport protein)
  • Ferritin (iron storage in liver, spleen, kidney, bone marrow)
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41
Q

Describe iron toxicity

A
  • Not common
  • Mainly with prolonged oral administration
  • Alimentary disturbances
  • Reduced growth
  • Induced phosphorous deficiency
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42
Q

In what scenarios is the iron requirement increased?

A
  • Pregnancy

- After prolonged haemorrhage

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43
Q

Describe iron deficiency

A
  • Main symptom anaemia
  • Suckling pigs
  • Poor appetite adn growth, breathing laboured and spasmodic (thumps)
  • Not common in calves or lambs
  • Sommetimes in laying hens due to drain of egg production on body reserves
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44
Q

Describe the metabolic roles of manganese

A
  • Major biocehmical role as activator of enzymes including hydrolases and kinases
  • Also constituent of arginase, pyruvate carboxylase and Mn superoxide mutase
  • Many interactions with choline
  • Perosis and fatty liver infiltration
  • Choline one of B serous vitamins
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45
Q

Outline the defiency problems associated with manganese

A
  • Ruminants, pigs, poultry
  • Retarded growth
  • Skeletal abnormalities (muscular weakness, perosis, lameness)
  • Ataxia of neonates
  • Reproductive failure
  • Impaired glucose utilisation
  • Reduced vitamin K blood clotting responses
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46
Q

Outline the toxicity problems associated with manganese

A
  • Wide safety margin between requirement and toxic doses
  • Not usually an issue
  • Depressed appetite
  • Reduced growth
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47
Q

Describe the major metabolic roles of zinc

A
  • Essential component of over 200 metalloenzymes
  • Carbonic anhydrase, pancreatic carboxylase, alcohol dehydrogenase, alkaline phosphatase, thymidine kinase
  • Activator of several enzyme systems
  • Cell replication and differentiation (RNA/DNA synthesis)
  • Production, storage and secretion of hormones
  • Immune system
  • Electrolyte balance
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48
Q

Outline the deficiency problems associated with zinc

A
  • Major dietary interaction siwth calcium and phytate
  • Also copper
  • Pigs fed high Ca rations (incl. phytate)
  • Subnormal growth, depressed appetite, poor food conversion and parakeratosis
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49
Q

What are the symptoms of zinc deficiency in calves?

A
  • Inflammation of nose and mouth
  • Stiff joints
  • Swollen feet
  • Parakeratosis
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50
Q

What are the symptoms of zinc deficiency in chicks?

A
  • Retarded growth
  • Foot abnormalities
  • Frizzled feathers
  • Parakeratosis
  • Swollen hock syndrome (bone abnormality)
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51
Q

Outline the problems with zinc toxicity

A
  • Most animals have high tolerance
  • Depressed good consumption
  • May induce copper deficiency
  • Zinc usually associated with protein content in diet
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52
Q

Describe the metabolic roles of iodine

A
  • 2 known roles
  • Thyroxin
  • Triiodothryonin
  • Are the thyroid hormones
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53
Q

Describe the roles of the thyroid hormones

A
  • Increase basal metabolic rate
  • Accelerate growth
  • Increase oxygen consumption
  • Control development of foetus
  • Involved in immune defence, muscle function, seasonality of reproduction
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54
Q

How are T4 (thyroxin) and T3 (triiodothryonin) produced?

A
  • Iodiine from iodides in blood coombine with tyrosine to produce monoiodotyrosine (T1) and diiodotyrosine (T2)
  • 2xT2 condense = T4
  • T4 is physiologically inactive transport form stored in thyroid gland
  • Released into blood as required
  • Converted into active T3 peripherally (mainly kidneys and liver)
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55
Q

What is the importance of selenium in iodine metabolism?

A
  • Deiodinase enzymes (T4 to T3) are selenium dependent

- Deficient in selenium, reduced iodine metabolism

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56
Q

Describe the symptoms of iodine deficiency

A
  • Enlarged thyroid gland (goitre) due to compensatory hypertrophy
  • Reproductive abnormalities
  • Underweight, hairless, weak or dead offspring
  • Cretinism
  • Oestrus suppressed/irregular
  • Reduced milk yield
  • male decreased libido, reduced semen quality
  • Poor wool growth
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57
Q

What may cause iodine deficiency?

A
  • Not supplying enough in diet
  • High amount of goitrogens (found in brassicas)
  • Thiocyanate competitive inhibition of iodine uptake, can be overcome by increased iodine supplementation
  • Goitrin inhibits iodination of tyrosine, cannot be overcome by increasing dietary iodine
  • High dietary nitrogen inhibits iodine uptake
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58
Q

Outline the problems with iodine toxicity

A
  • Depressed weight gain and feed intake
  • Decreased egg production
  • No effect on fertility of effs but early embryonic mortality
  • Reduced hatchability and delayed hatching
  • Pigs more tolerant
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59
Q

Describe the major metabolic roles of molybdenum

A
  • Involved in a few metalloenzymes
  • Xanthine oxidase
  • Aldehyde oxidase
  • Sulphite oxidase
  • Cogactor in reaction of xanthine oxidase with cytochrome C
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60
Q

Outline the deficiency problems associated with molybdenum

A

Has not been observed in any species under natural conditions

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61
Q

Outline the toxicity problems of molybdenum

A

Interactions with copper

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62
Q

Describe the major metabolic roles of chromium

A
  • Essential for normal glucose utilisation
  • Role in lipid synthesis
  • Protein and nucleic acid metabolism
  • Improves appetite weight gain and humoral immune response in recently moved and vaccinated (stressed) calves
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63
Q

Outline the deficiency and toxicity problems with chromium

A

Not particularly toxic

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64
Q

Describe the major metabolic roles of lead

A

No metabolic role

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65
Q

Outline the toxicity probelms associated with lead

A
  • Acute leads to GI haemorrhage, anaemia, kidney damage and liver necrosis
  • Chronic leads to osteoporosis, hydronephrosis, loss of appetite and “lead lines”
  • Suckling lambs/young calves vulnerable
  • Reduced learning
  • Often from paint, old batteries, sewage sludge, mining activities
66
Q

Describe the major metabolic roles of cadmium

A

No metabolic role

67
Q

Outline the toxicity problems associated with cadmium

A
  • Highly reactive and toxic
  • Antagonistic interactions with copper and zinc (increased zinc decreases Cd absorption)
  • Accumulates in liver and kidney
  • Sources: superphosphate fertilisers, sewage sludge
  • Can lead to decreased appetite, fertility and libido
68
Q

Describe the major metabolic roles of fluorine

A

Tooth strength

69
Q

Outline the deficiency problems associated with fluorine

A

No natural deficiency in farm animals

70
Q

Outline the toxicity problems associated with fluorine

A
  • Ruminants more susceptible
  • Dental pitting and wear
  • Depressed appetite
  • Lameness
  • Reduced production
  • Bone and joint abnormalities
  • Sources: fluoride containing water, industrial pollution, use of soft/raw rock phosphate supplements
71
Q

List the vitamins of the B complex

A
  • Thiamin
  • Riboflavin
  • Nicotinamide
  • Pyridoxine
  • Pantothenic acid
  • Biotin
  • Folic acid
  • Choline
  • Cyanocobalamin
72
Q

Describe the vitamine B complex

A
  • All water soluble
  • Most components of co-enzymes
  • Not stored in tissues
  • Regular dietary supply essential
  • In ruminants can generally be synthesised by bacteria in rumen
  • Also bacteria in gut of horse
  • By caecal fermentation
  • Ingested through coprophagy in rabbits
73
Q

Describe the role vitamin B1 - thiamin

A
  • Coenzyme thiamin pyrophosphate
  • Oxidative decarboxylation of pyruvate to acetyl CoA (lactate accumulation)
  • Oxidative decarboxylation of alpha-ketoglutarate to succinyl CoA in TCA cycle
  • Transketolase in pentose phosphate pathway
  • Thiamin triphosphate involved in activation of Cl channel in nerve cell membranes
74
Q

Describe the role vitamin B2 riboflavin

A
  • Flavoproteins
  • All involved in transport of H reactions
  • Oxidative phosphorylation
  • Succinic dehydrogenase (TCA cycle)
75
Q

Describe nicotinamide

A
  • AKA niacin, nicotinic acid
  • Very stable
  • Synthesised from tryptophan, low dietary requirement, conversion rates can be low
  • Cats need preformed source (cannot synthesise)
  • Active group os 2 important co-enzymes
  • NAD and NADP
76
Q

Describe B6 pyridoxine

A
  • Consists of 3 readily interchangeable forms
  • Pyridoxine (most stable)
  • Pyridoxal
  • Pyridoxamine
  • Mainly functions as pyridoxal phosphate
  • Over 50 of these
  • Transamination adn decarboxylations
  • Role in absorption of AAs from intestine
77
Q

Describe pantothenic acid

A
  • Consituent of CoA
  • Energy metabolism
  • Widely distributed vitamin
  • Deficiency rare in practice
78
Q

Describe the role of biotin

A
  • Prostethic group for 3 important enzymes
  • Pyruvate carboxylase
  • Acetyl CoA carboxylase
  • Proprionyl CoA carboxylase
79
Q

Describe folic acid

A
  • Converted to tetrahydrofolic acid
  • Coenzyme for mobilisation and utilisation of single carbon groups (methyl, formyl) (histidine, serine, glycine, methionine, purines)
  • Involved in synthesis of RNA, DNA and neurotrasmitters
  • Green leady veg and cereals good natural sources
  • stable under dry conditions, degraded by moisture and UV light
80
Q

Describe choline

A
  • Unlike other B vits not metabolic catalyst/cofactor
  • Component of lecithin
  • Important role in lipid metablism
  • Prevent accumulation of fat by converting excess fat into lecithin
  • Increase utilisation of fatty acids
  • Component of ACh
  • Donor of methyl groups for transmethylation reactions involving B12 or folic acid
  • Methionine or betaine can replacce choline as methyl donor but not other functions
81
Q

Describe B12 cyanocobalamin

A
  • Almost exclusively microbial origin
  • Requires specific glycoprotein (intrinsic factor) to bind in intestine for absorption
  • Many metabolic roles
  • Isomerases, dehydrases, enzymes for synthesis of methione from homocysteine, methylation
  • Proprionate metabolism
82
Q

Describe the deficiency symptoms of B1 thiamin

A
  • Loss of appetite
  • Emaciation
  • Muscular weakness
  • Progressive dysfunction of nervous system
  • Widely distributed in foods so deficiencies rare
83
Q

Describe the deficiency symptoms of B2 riboflavin

A
  • Deficiencies rare in ruminants (synthesised in rumen)
  • Loss of ppetite, diarrhoea, lesions in the corners of mouth
  • Iin pigs required for normal oestrus activity and prevent premature parturition
  • Poor appetite, growth retardation, vomiting, skin eruptions adn eye abnormalities
  • In poultry chicks “ curled toe paralysis”, reduced hatchability and embryonic abnormalities
84
Q

Describe deficiency in nicotinamide

A
  • Ruminal supplementation may reduce ketosis in early lactation
  • May be low in maize diets
  • In pigs leads to poor growth, anorexia, enteritis, vomiting, dermatitis
  • In poultry leads to bone disorders, feathering abnormalities, inflammation of mouth and upper oesophagus
85
Q

Describe B6 pyridoxine deficiencies

A
  • Results in large variety of biochemical lesions
  • Predoominantly related to AA metabolism
  • Widespread distribution of pyridoxine in plants so deficiency unlikely
86
Q

Describe pantothenic acid deficiencies

A
  • Widespread vitamin so deficiency rare
  • Some reports in commercial pigs
  • Slow growth, diarrhoea, hair loss, scaliness of skin, “goose-stepping” gait
87
Q

Describe biotin deficiencies

A
  • Widely distributed, availability low in P&P from some feeds incl barley adn what
  • In pigs leads to foot lesions, alopecia, dry scaly skin, decreased growth rate, decreased food utilisation, decreased reproductive performance in sows
  • In poultry leads to reduced growth, dermatitis, legbone abnormalities, cracked feet, poor feathers, fatty liver and kidney syndrome
88
Q

Describe folic acid deficiencies

A
  • Chickas and youg turkeyrs

- Poor growth, anaemia, poor bone development, poor egg hatchability

89
Q

Describe choline deficiencies

A
  • Methionine or betaine can replace choline as methyl donor but not other functions
  • Synthesised in liver from methionine
  • Exogenous requirement influenced by methionine in diet
  • Requirement high
  • Deficiency rare
  • Can lead to slow growth, fatty infiltration of liver
  • Manganese interacts with choline
90
Q

Describe B12 cyanocobalamin deficiencies

A
  • Adult animals less suscpetible
  • Young have growth retardation and high mortality
  • In young pigs poor growth, lack of hind leg coordination
  • In older pigs dermatitis, rough oat, sub-optimal growth
  • In poultry decreased growth, poor feathering, kidney damage, decreased hatchability
  • In ruminants related to cobalt, decreased growh, decreased appetite, anaemia, emaciation, pica often exhibted
  • In horses linked to cobalt
91
Q

Explain why ruminants do not need a dietary source of B complex vitamins

A
  • Can be synthesised by bacteria in rumen

- Cobalt required in vit B12 production

92
Q

Explain how some compounds can act as vitamin antagonists

A
  • Thiaminase
  • Antagonist to thiamin
  • Present in bracken, raw fish
  • bacterial thiaminase may be induced by acidotic conditions in rumen (rapid fermentation)
  • Can lead to circling movements, head pressing, blindness, muscular tremors
  • In poultry may cause paralysis, stargazing, fatty liver and kidney
93
Q

Outline cobalt and its interaction with B12

A
  • Needed to produce B12
  • Most B12 deficiencies caused by cobalt deficiency initially
  • Also has role as activating ion in certain ensyme reactions
  • Cobalt poorly retained in animal
  • Even if a lot of cobalt provided, will not dramaticaly increases production of B12
  • Bacteria need time to adjust to high dose of cobalt
  • Some used, some excreted
  • Uptake into animal is quick
  • Cobalt in blood not useful for B12 production, need slow release source
94
Q

Why is high cobalt in the blood useful in racehorses?

A
  • Good for oxidative carrying in blood
  • Increases stamina
  • Is therefore banned in racehorses
95
Q

List sources of vitamin A

A
  • Fish liver oil
  • Egg yolks
  • Milk fat
96
Q

Describe precursors for vitamin A

A
  • Certain carotenoids in plants
  • Converted to vit A
  • 2 main categories: carotene and xanthophils
  • Lots of different xanthophils
  • Main vit A source in ruminants is beta carotene
  • Different conversion eggicacies in different species
  • Cats do not have enzyme to convert carotene to vit A, need dietary source
97
Q

Where is vitamin A stored?

A

The liver

98
Q

What can be used to assess the amount of vitamin A present?

A
  • Serum retinol
  • Retinyl ester concentrations
  • Liver biopsy
  • Clinical signs and diet
99
Q

List the sources of vitamin C

A
  • Citrus fruits
  • Green leafy vegetables
  • No precursors
100
Q

How can vitamin C be synthesised

A
  • From glucose via glucoronic acid and gulonic acid using L-gulonolactone enzyme
  • No store of vit C
  • Cannot be synthesised by guinea pigs or primates
101
Q

How can vitamin C status be assessed?

A
  • Low liver and kidney concentrations
  • In fish - vertebral collagen level
  • Blood tests and x-rays
  • Clinical signs (reduced healing etc)
102
Q

List the sources of vitamin D

A
  • Fish liver oil
  • Sundried roughage
  • Egg yolk
103
Q

List the precursors of vitamin D

A
  • Animal derived vitamin D3 (cholecalciferol) or plant derived D2 (ergocalciferol)
  • Are precursors for calcittriol
  • D3 activated by UV
  • Skin vit D (7-hydroxycholesterol)
  • Cholecalciferol goes on to form calciferol, which goes on to form active calcitriol
104
Q

Describe the synthesis of D3

A
  • Humans can synthesise from UV
  • Cats and dogs lack enzyme that converts precursor to cholecalciferol so cannot synthesise from UV
  • Skin vit D (7-dehydroxycholesterol) converted to D3 using UV
105
Q

Where is vitamin D stored?

A

Liver

106
Q

How can vitamin D status be assessed?

A
  • Measurement of low serum 25(OH)-D3
  • Ionised calcium concentrations
  • Increased PTH concentration
107
Q

Describe symptoms of vitamin D deficiency

A
  • Rickets
  • Puppies lethargic
  • Poor muscle tone, bowing of limbs
  • Clinical signs of calcium deficiency in adults (take time to develop)
  • Kittens have poor food intake, lose weight, generalised ataxia, caudal paralysis
  • Young catle arched back, swollen hocks
  • Pigs enlarged joints, broken bones, stiff joints, adversely affected growth rates, occasionally paralysis
  • Poultry bones and beak soft and rubbery, legs weak, reduced egg production with poor shell quality
108
Q

Describe the metabolic role of vitamin A in the eye

A
  • Retinol converted to 11-cis isomer, oxidised to 11-cis-retinaldehyde
  • Used to see in the dark
  • Combines with opsin to form rhodopsin
  • Photoreceptor for light at low light intensities
  • Retinal is same as 11-cis-retinaldehyde
109
Q

Describe the metabolic role of vitamin A in general system

A
  • Regulation of cellular differentiation
  • Formation adn protection of epithelial tissues and mucous membranes
  • Important in growth, reproduction adn immune response
  • Also important in resistance to disease and promotion of healing through its effect on immune system and integrity of epithelium
110
Q

Describe the symptoms of vitamin A deficiency

A
  • Blindness
  • Epithelial infection
  • Night blindness
  • Roughened hair, scaly skin
  • lambsborn weak or dead
  • In poultry mortality rate high, retarded growth, ruffled ploumage, staggers
  • Dogs: ataxia and anorexia
  • cats: reproductive and developmental disorders
111
Q

Describe the major metabolic roles of vitamin C

A
  • Oxidation reduction mechanisms in living cells
  • Cofactor for these
  • Needed for maintenance of normal collagen metabolism
  • Cofactor for hydroxylation
  • Plays role in transport of iron-ions from transferring to ferritin
  • Antioxidant, ascorbic acid works with vit E in protecting cells from oxidative damage caused by free radicals
112
Q

Describe the symptoms of vitamin C deficiency

A
  • Reduced resistance to infection
  • Failure in collagen formation - strucural defects
  • Wound healing at slower rate
  • Those that do not synthesise more at risk
113
Q

Describe the major metabolic roles of vitamin D

A
  • Similar to steroid
  • DNA transcription in microvilli
  • Induce synthesis of specific mRNA
  • Repsonsible for production of calcium binding protein
  • Amount produced by kidney controlled by PTH
  • Calciferol increases absorption of phosphorous from intestines
  • Enhances calcium and phosphorous reabsorption from the bone
114
Q

What may predispose a cow to hypomagnesaemia?

A
  • Low magnesium intake
  • Older cow
  • Ingestion of high levels of potassium and nitrogen (fertiliser)
  • Spring calving
  • Eating rapidly growing grass
  • Consistently stormy wet weather meaning does not eat
  • More crude protein in grass disrupting microflora
115
Q

Explain how magnesium affects calcium metabolism

A
  • Compete for transport mechanism
  • Less magnesium means more calcium influx into nerve endings
  • Increased release of ACh leading to tetany
  • Low magnesium reduces PTH
  • More Ca into urine
  • Low magnesium => less competition => high calcium => less PTH released leading to decreased resorption from bone, increased excretion in urine
116
Q

Explain how potassium affects magnesium absorption

A
  • High potasium leads to reduced uptake
  • Leads to apical membrane depolarising
  • Reduces transepithelial potential
  • Does not propel rumen magnesium into blood
117
Q

Explain how sodium affects magnesium absorption

A
  • Low sodium leads to reduced uptake
  • Sodium-linked ATP-ase dependednt transporter
  • Low sodium cannot generate concentration gradient
  • Sodium not drawn into cell to be pumped out on other side
  • As sodium is drawn into cell, magnesium would be taken with it (symport)
118
Q

Where is magnesium absorbed in the ruminant and non-ruminant?

A
  • Ruminant: rumen

- Non-ruminant: small and large intestine

119
Q

List some of the important nutritional interactions

A
  • Sodium-potassium
  • Calcium-magnesium
  • Manganese-iron
  • Iron-copper
  • Zinc-copper
120
Q

What may cause a high iron content of forage?

A
  • Acidic soil
  • Compacted and anaerobic
  • Contamination of crop in harvest time
121
Q

What are some of the analytical methods available for assessing mineral status?

A
  • Rate/endpoint assays

- Feed testing

122
Q

What are soe suitable samples for assessment of mineral status?

A
  • Serum and whole blood
  • Milk
  • Urine
  • Post mortem sample of liver
123
Q

What is serum an appropriate sample to test the status of?

A
  • All macro- and microminerals
124
Q

What is urine an appropriate sample to test the status of?

A

P, Cl, Na, Pb

125
Q

What is the liver an appropriate sample to test the status of?

A

Fe, Se, B, Mn complex vitamins, Cu

Co by testing levels of B12 in th liver

126
Q

What is whole blood an appropriate sample to test the status of?

A

Cl, Mn, Pb Se

127
Q

Describe the major metabolic roles of selenium

A
  • Mainly incorporated into antioxidant enzyme glutathione peroxidase
  • Immune response
  • Iodine metabolism
  • Metabolism of sulphydral compounds, fatty acids and glucose
  • Interacts with vitamin E
128
Q

How does selenium affect iodine metabolism?

A
  • Deiosinase enzymes are selenium dependent
  • Iodothyronine deiodinase is crucial for thyroid function
  • Converts thyroxin/T4 inactive form to T3 active form
129
Q

Describe the major metabolic roles of vitamin E

A
  • Membrane bound antioxidant
  • Immune system
  • Not stored in the body
  • Interactions with selenium
  • a,b,x,d - tocopherols (greek letters) - saurated form
  • a-tocotrienol also has vitE activity - unsaturated form
130
Q

Describe the interaction between selenium and vitamin E

A
  • Are mutually replaceable
  • Maintains Se in body in active form (GSHPx form)
  • Prevents destruction of lipid membranes, inhibiting production of peroxides
  • Therefore lowers requirement of GSHPx
131
Q

Describe the metabolic roles of copper

A
  • Metalloenzymes
  • Activator of several enzyme systems
  • Development of CNS and heart
  • Energy and iron metabolism
  • Immune sysem
  • Pigment and connective tissue formation
  • Antioxidant
132
Q

List some of the important copper enzymes

A
  • Tyrosinase
  • Cytochrome oxidase
  • Lysyl oxidase
  • Superoxidase dismutase
  • Caeruloplasmin
133
Q

What is the action of tyrosinase?

A

Conversion of amino acid tyrosine to black pigment melanin

134
Q

What is the action of cytochrome oxidase

A

Electron transfer chain (reduces energy utilisation)

135
Q

What is the action of lysyl oxidase

A
  • Collagen adn elastin cross linkage
136
Q

What is the action of superoxidase dismutase

A

Antioxidant and immune function

137
Q

What is the action of caeruloplasmin

A

Blood copper transport system and oxidant of Fe II to Fe III for incorporation into haem

138
Q

Describe the metabolic role of magnesium

A
  • Close metabolic associations with Ca and Phos
  • 70% in skeleton, rest highly metabolically active
  • Most common enzyme converter
  • FOrmation of cyclic AMP
  • Cellular respiration, forms complexes with ATP, ADP and AMP
  • Moderate neuromuscular activity
139
Q

Describe deficiencies in magnesium

A
  • Many species
  • Depleted bone magnesium, tetany, death
  • Main problems are in ruminants (hypomagnesium tetany/grass staggers)
  • In ruminants major absorption from rumen decreased by potassium
140
Q

What are the symptoms of selenium deficiency?

A
  • White muscle disease
  • Ill thrift, reduced groth rates, decreased wool
  • Impaired immune function
  • Decreased reproductive performance
  • In pigs: mulberry heart, hepatosis dietetica
  • In poultry: pectoral myopathy, encephalomacia, exudative diathesis, pancreatic fibrosis
  • Stiff but weak
141
Q

What are the symptoms of selenium toxicity?

A
  • Alkali disease, blind stagger
  • Fullness, lack of vitality, rough coat, hair loss, soreness/sloughing of hooves
  • Stiffness/lameness, sudden death
  • Areas of high Se or Se accumulator plants can cause this
142
Q

How can selenium in the body be assessed?

A
  • Blood Se

- GSHPx

143
Q

Describe the symptoms of vitamin E deficiency in pigs

A
  • Muscular myopathy

- Mulberry heart disease

144
Q

Describe the symptoms of vitamin E deficiency in poultry

A
  • Mainly pectoral myopathy
  • Encephalomacia
  • Exudative diathesis
145
Q

Describe the symtoms of vitamin E deficienc in the horse

A
  • Lameness and muscle rigidity from muscle myopathy
  • Red blood cell fragility
  • Myoglobin release to urine (coffee colour)
146
Q

Describe the symptoms of copper deficiency in non-ruminants

A
  • Rare in non-ruminants
  • Copper related anaemia can occur when milk only diet
  • Older animals deficiency unlikely
  • In cats leads to poor reproductive performance, kittens small, weak, discoloured and curly coats
147
Q

Describe the symptoms of copper toxicity in non-ruminants

A
  • Cumulative poison
  • Pigs highly tolerant
  • Can lead to growth retardation
  • Haemolytic crisis not as pronounced
  • In poultry can lead to erosion of gizzard
148
Q

Outline the deficiency problems associated with copper in ruminants

A
  • Swayback
  • Hair/wool keratinisation and depigmentation
  • Bone disorders
  • Anaemia
  • Infertility
  • Immune function impaired
  • Lipid metabolism and oxidative stress
  • Impaired glucose metabolism
  • Lots of processes in rumen, interactions leading to deficiency
  • Thiomolybdate toxicity leads to copper deficiency
149
Q

Describe how thiomolybdate toxicity leads to copper deficiency

A
  • Mo (molbdenum) binds to sulphide
  • If does not bind to copper, absorbed into tissues from rumen as MoS
  • Copper in an enzyme, MoS binds, changes shape of enzyme, action prevented by altering active site
  • More sulphur in MoS, more affinity for copper
  • In intestine, Cu, Fe form complex, insoluble, passedin urine
  • CuMoS4 passed in urine
  • Copper lock up, not absorbed
  • Cu absorbed into tisues
  • MoO4 (molybdate) absorbed into tissues, will not bind to Cu
  • If copper and thiomolybdate are absorbed separately then bind, affects enzyme activity
  • CuMoS4 and Cu can go to the liver
150
Q

Outline the toxicity problems associated with copper in ruminants

A
  • Mainly problem if over or inappropriate copper supplementation
  • Copper toxicity itself not reported to affect reproduction
  • Long term thiomolybdate treatment of copper toxicity does cause infertility
  • Se supplementation in sheep and goats predisposes to increased risk of copper toxicity
  • Copper loaded in liver, need stress trigger togo from copper loaded to copper toxic
151
Q

What are the signs of copper toxicity in ruminants

A
  • Weak
  • Tremulous
  • Listless
  • Anorexic
  • Haemolytic crisis breakdwon of haemoglobin into urine and plasma
152
Q

Describe the diagnosis of copper toxicity and deficiency in ruminants

A
  • Liver enzymes AST, GGT

- Liver already damaged when these rise!

153
Q

Describe the treatment of copper toxicity in ruminants

A
  • Injection of ammonium tetrathiomolybdate (not recommended!)
  • Zinc therapy
  • Feeding of other antagonists
  • Iron, molybdenum, zinc
154
Q

How is sheep breed linked to copper deficiency/toxicity?

A
  • Depending on breed predisposed to deficiency/toxiciy
  • Historical location
  • Lots of copper naturally present = more likely to be deficient
  • Not much copper present = more likely to become toxic
  • Swaledale, scottish blackface, charollais deficient
  • Suffolk, texel, bluefaced leicester usually no problems
  • North ronaldsey toxic (eat seawweed, seaweed low in copper)
155
Q

How can the macromineral status of an animal be assessed?

A
  • Serum levels (not always accurate, levels homeostatically regulated)
  • Feed
  • Urine
156
Q

How can the trace mineral status of an animal be assessed?

A
  • Feed
  • Serum, plasma, whole blood (no homeostatic regulation!)
  • Functional indicators (enzymes, vitamins, cobalt for B12)
  • Milk (not great, changes in “cycle”)
157
Q

How can the vitamin status of an animal be assessed?

A
  • Not many tests available
  • Mainly B12, sometimes B1
  • Assess functional indicators
  • Don’t tend to get deficiencies, may be expensive
158
Q

How can copper status of an animal be assessed?

A
  • Plasma copper up, function down

- PLasma copper, TCA solube copper, caeruloplasmin superoxide dismutase haemoglobin/haematocrit

159
Q

How can vitamins and minerals be supplemented

A
  • Bolus (slow release)
  • Free access lick (nt always effective)
  • In feed
  • Added to water
  • Injection
  • Liquid drench
  • Use of certain fertilisers
  • Changing crops
160
Q

Describe chelates

A
  • A compound containing a ligand (typically organic) bonded to a central metal atom at 2 or more points
  • Some minerals bound to proteins of enzymes, others present in prosthetic groups in chelated form
  • E.g. chlorophylls, cytochromes, haemoglobins, vitamin B12

GI (31 decks)

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