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20 Cards in this Set
- Front
- Back
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What is the pathogenesis of osteomalacia?
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Osteomalacia
•Efficient P and Ca absorption requires adequate vitamin D (forms 1,25-DHCC –regulates phosphate in the kidneys). •High dietary Ca intake depresses P absorption. If cattle have adequate Ca intake but inadequate P, P absorption is decreased. •Vitamin D deficiency can occur in winter on fast growing cereal crops. Oats can have a vitamin D inhibitor |
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Coxofemoral luxation(dislocated hip). How do you treat it?
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•Sedate with 1mL xylaxine
(100mg/mL) •Pass a rope though the inguinal area and tie to a fence behind the cow •Connect a second rope to a pulley above and below the right hock •Thread a batton (wooden dropper) through the rope over the hock •Apply traction caudo-ventrally using pulley while simultaneously rotating stifle inwards and hock outwards •For difficult cases, may need deeper muscle relaxation (Guaifen® (glyceryl guaiacolate) IV in addition to the xylazine already injected) • Off label – a little risky but may be no other option • 10 day milk WH, 30 day meat WH |
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most useful single
prognostic factor for hips are ? |
Jubb et al found the most useful single
prognostic factor was whether the cow was able to stand before the reduction. Other positive factors included age < 3years, BW < 400kg and duration < 12 hours |
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What is the response of a hpocalcemia cow to treatment?
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•Belching
•Muscle tremors •↑amplitude and pressure of the pulse •↑heart sound intensity •Defaecation and urination •Sweat beads on the muzzle and lacrimation starts |
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HOw do you px relapses?
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Drench cow with oral calcium chloride (eg Calcoral Gel®) for 2 -3 days after initial treatment
•Do not milk the cow right out (48 hrs) •Don't allow the calf unlimited access •If cows remain down after treatment ensure access to feed and water, non-slip bedding, sit in sternal not lateral recumbency. |
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What would you recomend to fix hypocalcemia in a herd? HOw long does the treatment extend for?
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•Feed a transition diet for 21 days before calving (if accurate calving dates)
•At least 10-14 days recommended •Do not feed for >21 days (increases milk fever risk again) Aim: To induce a mild metabolic acidosis -↑calcium mobilisation from bone and enhances Ca absorption from intestine. |
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What is the aim of the springer diet?
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DifferenceSpringers aim: negative DCAD (or close to it)Suggested range +5 to -5 meq/100g DMGoal –induce mild metabolic acidosis to reduce risk of hypocalcaemiaAlmost
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What is the goal of the cow diets?
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Neutralise the acids from rumen fermentation and systemic metabolism.
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What diets do you recommend?
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•Do not feed kikuyu pasture
•Change lucerne hay to oaten hay •Remove sodium bicarb from the grain mix fed to the transition cows •Add anionic salts (eg. ammonium sulphate, magnesium sulphate) …or feed brewers grain •Ensure adequate Mg in the diet |
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what are the factors contributing to hypomagnesemia?
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Seasonal changes
•Winter calving cows are at greatest risk -cold, lush pastures low in soluble CHO, high in N and fats. They also have an increased demand for Ca and Mg in milk. Phosphorus and calcium •Low rumen P conc. impairs Mg absorption •Cows with hypomagnesaemia do not develop grass tetany until blood calcium levels decrease •Cows absorb less Ca from pasture during winter when grass is immature |
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what are the clinical singns of hypomagnesemia?
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•Stop grazing, very alert (twitching of ears and muzzle)
•Animals may gallop in a wild frenzy or charge •Progression to staggering, lateral recumbency with frantic paddling and clonic tonic convulsions •Opisthotonus and nystagmus •Champing of jaws and clicking of eyelids •Head arches, mouth frothing •Temp 41C, sweating, ↑HR & RR •Death 30 –60 min, mortality high |
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How do you diagnose mypomagnesemia?
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Necropsy -collect serum (cardiac puncture), CSF, urine ( up to 12 hrs after death) and an enucleated intact eye for aqueous or vitreous humor(up to 48 hours after death if temp <23oC)
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How do you treat hypomagnesemia?
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Replacement Therapy
•Mg hypophosphate IV •(Off label -5% Mg sulphate (Magnesate™) diluted in 1 litre of saline and given IV) •Monitor the heart throughout treatment. Mg salts are toxic and can result in respiratory failure when given IV –give slowly Give Mg-Ca combinations if suspect animal is also hypocalcaemic Expect clinical improvement within 3 –5 hours •Warn owner cow may die during a convulsion even after prior treatment. Relapses are common within 3 –6 hrs of tx •Give MgSO4SC or “Cal-Jet Oral®” PO •Provide legume hay if possible Sedation therapy •If convulsions seen, sedate cow if possible •IV chloral hydrate may prevent convulsions while exogenous Mg takes effect •Put animal in sternalrecumbency |
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what is the daily requirements of magnesium of cattle?
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•Daily Mg requirement for cattle is 30 –40 g/hd/day
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what is the ways for preventing hypomagnesemia?
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•Avoid grazing cattle on new grass until it is 4 –6 inches tall (matures)
•Graze mixed legume-grass pastures (> 20% clover) and feed legume hay. •If no legume hay available, any hay, straw or silage will reduce rumen flow rates and increase absorption of Mg and Ca. •Identify high risk paddocks and graze with low risk stock. Early lactating cows most at risk. Feed a Mg supplement •Provide shelter against inclement weather •Avoid calving older cows in the winter and manage older fat cows in a separate high risk group. •Mg fertilizer and dolomitic limestone can be applied to the soil to increase Mg concentration in plants. •Dusting pastures with MgO increases Mg intake but is often not cost effective |
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What is ketosis?
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Multifactorial disorder of energy metabolism
Breakdown products of fat metabolism accumulate in the body fluids Characterised by: •Hypoglycaemia •Ketonaemia •Ketonuria Usually occurs in the first 6 weeks of lactation Can affect a large proportion of the cows in early lactation in a herd. |
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What is the risk factors for ketosis?
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Risk factors include:
•Periparturient period (<60 days post calving) •Increased age (peak incidence 3rd–6thlactation) •Increased milk production •Low energy, high protein diets •Obesity at calving •Occasionally prepartum -twin bearing cows on low energy diets are at increased risk |
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What are the 3 scenarios that predispose hypomagnesemia?
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Alimentary ketosis
•Excessive intake of butyrate in silages and possible inappetance ** check diet Primary underfeeding •Poor BCS + poor-quality feeds = limited gluconeogenesis from feed. •Low dietary crude protein is associated with decreased fermentation rates and DMI ** check diet to ensure adequate CP Secondary underfeeding A decrease in voluntary feed intake due to underlining disease eg. acidosis on a herd scale. ** check lactating cow and transition cow diet for explanations ofunderlying disease |
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How would you treat ketosis?
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Replacement therapy:
Propionate precursors PO (eg. propylene glycol) +/-IV glucose therapy |
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What adjunctive therapy can you supply to treatm hypomagnesemia?
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•Corticosteroids –commonly used
•Cause decreased peripheral utilisation of glucose in muscle and fat and increased Acetyl CoA utilisation •Anabolic steroids -decrease blood ketone levels and stimulate appetite •Protamine Zn Insulin may be useful •B Group Vitamins –Niacin increases blood glucose and decreases blood ketones •Digestive tract stimulants such as Clanobutin Sodium (Bykahepar) may help a poor appetite Treatment Corticosteroids •Appear to cause decreased peripheral utilisation of glucose in muscle and adipose tissue and increased acetyl Co-A utilisation (repartitioning of glucose rather than gluconeogenesis). •Causes hyperglycaemia within 24 hours of administration •40mg dexamethasone sodium phosphate can produce hyperglycaemia in ketotic animals for 4 –6 days Insulin •Zn Protamine promotes cellular uptake of glucose, suppresses fatty acid metabolism and stimulates hepatic gluconeogenesis |
