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15 Cards in this Set

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Factors influencing absorption of dietary copper
Sulphur
Molybdenum
Iron
Intercurrent disease
Genetics
Who is suceptible to copper deficiency?
Cattle more so than sheep
Young animals (esp. after weaning: 3-12 months of age)
Young of deficient dam
Animals grazing outdoors with no supplementation
Clinical signs
Depigmentation: greying of coat in dark cattle, esp. round eyes
Defective keratinisation: dry sparse hair coat
Bone defects: widening of the epiphyses of distal limb bones -> swollen fetlocks, spontaneous fractures, joint stiffness
Ill-thrift
Anaemia (of chronic disease)
Diagnosis
Clinical signs (non-specific except for swayback)
Dietary levels: of molybdenum, sulphur and iron ONLY (dietary levels of copper itself USELESS)
Plasma/serum copper levels: suitable for dx of clinical dz but not body copper reserves
Liver copper levels: by biopsy, rarely done except maybe at PM
Superoxide dismutase: expensive
Response to tx: cattle ONLY (risk of toxicity in sheep)
Caeruloplasmin: copper ratios?
Therapy
Direct
Oral: oral copper sulphate, copper oxide needles, intra-ruminal boluses
Injectable: EDTA, heptonate etc.
Inclusion in feed: banned in sheep although most concentrate feeds will have low levels
Free access minerals: cattle only?
Medication of water supply: cattle only

Indirect
Application of mineral fertilizer to pasture
Minimising molybdenum and iron intakes (e.g. by reducing soil intakes)
Genetic selection?
Role of selenium and vitamin E
Protect cells against damage by lipid peroxidases and free radicals.
Failure of this protection leads to MEMBRANE DAMAGE and TISSUE NECROSIS.
Tissues with highest rate of oxidative metabolism (i.e. skeletal, cardiac and respiratory muscle) most suceptible
Influencing factors
Selenium status
Supply of other dietary anti-oxidants (primarily VITAMIN E)
Supply of dietary oxidants (esp. polyunsaturated fatty acids - found in young rapidly growing pastures)
Generation of oxidants (e.g. via exercise at turnout, infection, toxins)
Clinical signs - WHITE MUSCLE DISEASE
Congenital
Stillbirths, weak calves that fail to suckle and usually die within a few hours

Delayed (usually precipitated by stress of turnout)
Skeletal m. - stiffness, discomfort, inability to stand, myoglobinuria
Respiratory m. - dyspnoea
Cardiac m. - sudden death (more common in pigs - mulberry heart disease)
Clinical signs - OTHER
Ill-thrift
Immunosuppression
Retained foetal membranes
Reduced fertility?
Diagnosis
Biochemical indicators of muscle damage (CK, AST)
Soil and pasture levels (useful UNLIKE OTHER TRACE ELEMENT DEFICIENCIES)
Selenium levels in blood and liver (short-term intake)
Glutathione peroxidase (GSHPx) levels in blood (long term intake)
Vitamin E levels in blood
Therapy
Direct
Oral compounds
Injectable compounds: short and long-term
Inclusion in compound feeds
Free-access minerals
Medication of water supply

Indirect
Application of selenium fertilizers to pasture
Causes of iodine deficiency
Primary
Low iodine content in soil (West of UK mostly)

Secondary
Ingestion of goitrogen containing plants (competitvely inhibit/prevent necessary conversion) e.g. brassicas, legumes (white clover etc)
Deficiencies of other trace elements (e.g. SELENIUM)
Environmental factors that increase BMR (e.g. low temperatures)
Clinical signs
Goitre
Stillbirths
Birth of weak calves/lambs
Poor production
Reduced fertility?
Diagnosis
Soil and pasture levels: not v. useful
Goitre
Thyroid histopathology: "gold standard"
Thyroid iodine levels
Iodine levels in blood, urine and milk
Thyroid hormone levels (care: natural variation)
Controlled supplementation trials
Therapy
Direct
Oral compounds
Injectable compounds: long-term
Painting of 5% tincture of iodine on the flank skin fold once a week (labour intensive)
Inclusion in compound feeds
Free-access minerals
Medication of water supply

Indirect
Application of iodine fertilizer to pasture
Minimise effects of goitrogens: thiocyanate - FEED MORE IODINE, thiouracil - AVOID FEEDING PLANTS CONTAINING IT