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What two other names is hepatic lipidosis in post-partum dairy cattle know by?

Fat Cow Syndrome and Lipid Mobilisation Syndrome.


What cattle are at risk of developing Fat Cow Syndrome?

Postparturient dairy cows which were overconditioned in the during late lactation and the dry period.
Obese/well conditioned cows with a large amount of omental and subcutaneous fat.


List the clinical signs of Fat Cow Syndrome.

Depression, anorexia, weight loss, weakness --> recumbency.
Non-specific signs may include decreased ruminal motility and milk production.
Other signs related to concurrent conditions e.g. mastitis, metritis, parturient paresis and displaced abomasum.


How do you diagnose Fat Cow Syndrome in a cow?

- Liver enzymes: often a poor indicator of dz severity; most consistently elevated are OCT, TBili, AST.
- CBC: often leukocytosis with a left shift (non-specific).
- Increased NEFAs and decreased cholesterol and triglycerides.
- BSP excretion > 9mins --> guarded Px.
- U/S: may see increased echogenicity of liver, rounded margins.
- Liver biopsy: % hepatocytes containing fat vacuoles - mild 75%. Liver will float in distilled water when >34% (NB all high-producing, post-parturient dairy cows will have fatty infiltration).


Describe post-mortem findings in a cow with Fat Cow Syndrome.

- Generalised obesity if sick


How do ruminants differ from monogastric animals in their intake of dietary energy?

- Most of the energy is absorbed is VFAs not glucose.
- Glucose is still needed and must be produced by gluconeogenesis, 85% of which occurs in the liver.


List conditions in which negative energy balance occurs in cattle.

- Lactation.
- Foetal growth.
- Exercise.
- Decreased feed consumption.
- Environmental chilling.
- Disease.


Describe the changes in insulin, glucose and hormone sensitive lipase (HSL) that occur in cattle during periods of negative energy balance or prior to lactation.

- Blood glucose concentration decreases.
- Insulin:glucagon ratio drops.
- Glucose, insulin, catcholamine, growth hormone changes activate HSL production.
- HSLs convert tissue fat to FFAs/NEFAs and glycerol.


What happens to the glycerol and NEFAs produced by breakdown of fat in cattle in negative energy balance?

- Glycerol --> liver --> produce glucose OR combine with FFAs to make triglycerides (TGs).
- FFAs --> combine w glycerol to make TGs OR degrated through beta-oxidation --> acetyl CoA --> krebs cycle --> glucose.
- If there is not enough oxaloacetate for acetyl CoA to combine with to enter the krebs cycle, acetyl CoA is converted to ketone bodies.
- NB ketones reduce feed consumption and perpetuate negative energy balance.


How does hepatic lipidosis develop in cattle with negative energy balance?

- When liver is overwhelmed with NEFAs greater amounts of TGs are deposited within hepatocyte.
- TGs eventually leave liver as VLDLs (plasma-soluble complexes of phospholipid, cholesterol and apolipoprotein A).
- Hepatic lipidosis occurs when rate of hepatic TG formation excedes oxidation of FAs and formation and release of VLDLs into peripheral circulation.


What dietary factors can increase the risk of hepatic lipidosis in cattle?

- Cows on low-protein diet in the dry period.
- Depression in DM intake in the final week before calving.
- Limiting feeding take of over-conditioned cows immediately after calving.


Is hepatic lipidosis a reversible condition in cattle?

Yes, if the cause is removed and the energy balance becomes positive (or less negative).


Outline treatment of hepatic lipidosis in cattle.

- Mild to mod: as for traditional ketosis.
- Severe: eliminate negative energy balance and factors/dz causing it:
-- Getting them eating is most imp; transfaunation may help.
-- IV glucose or insulin --> induces an insulin:glucose than will dec HSL mobilisation of FAs and stim prod of VLDLs.
-- Glucocorticoids IV/IM + glucose precursors orally e.g. propylene glycol, glycerol.
-- Choline: precursor of lipoproteins may inc rate of VLDL prod (not IV --> neuromuscular blockate); no controlled studies.
-- Nicotinic acid (niacin) may reduce lipolysis at the tissue level and the amount of fat presented to the liver.


What are the key pre- and post-parturient risk factors for development of hepatic lipidosis in dairy cattle?

- Pre-parturiet: obesity (BCS > 3/5), severe feed restriction, feeding excess energy, long calving interval.
- Post-partum: concurrent dz, anorexia or fasting, feed restriction, sudden feed changes.


Outline methods to prevent hepatic lipidosis in cattle.

- Prevent over-conditioning during the late lactation and dry periods.
- Tx peri-parturient dz early and aggressively.
- Adequate protein in dry period essential; good quality roughage (hay/silage).
- Commence feeding grain 2-4wks pre-partum to allow rumen to adapt to lactation diet; do not overfeed! Dm intake should be approx 2% BWt/day.
- Supplement dry cow ration w cobalt = precursor of vit B12 = co-factor in rate limiting step in conversion of propionate to succinyl CoA and thus glucose prod.
- Dry cow and lactating ration incl nicotinic acid to aid in dev of ketosis = primary risk factor for hepatic lipidosis.
- Monensisn in dry cow and early lactating ration may aid in prevention of ketosis.


Outline the signalment of cattle most at risk of Protein-Energy Malnutrition (PEM) and Pregnancy Toxaemia.

- Diseases of beef cattle on marginal diets.
- Growing, pregnant heifers are at greatest risk as energy requirement of growth are superimposed on other calorie requirements.


List risk factors for development of PEM and Pregnancy Toxaemia in beef cattle.

- Winter season e.g. snow cover.
- Unpalatable feed.
- Poor quality feed.


List clinical signs of PEM and Pregnancy Toxaemia in beef cattle.

- Weight loss/poor BCS.
- Weakness +/- inability to rise but still alert.
- Depression.
- Long hair coat.
- Body temp normal or hypothermic.
- +/- diarrhoea.
- Death usually occurs 7-14d after becoming recumbent.


Outline diagnostic test findings in beef cattle with PEM or Pregnancy Toxaemia.

- Demonstrating dec caloric intake + ruling out other chronic dz e.g. Johne's, lymphoma, parasitism.
- +/- hypoCa, anaemia, dec serum insulin conc.
- Ketonuria is not typical in PEM.
- Necropsy: dec muscle mass, atrophy of fat; fatty liver if acute or small liver if more chronic.


Describe treatment of PEM and Pregnancy Toxaemia in beef cattle.

- Treatment is often unrewarding.
- IVF, improve energy balance, tx concurrent dz.
- IV glucose, forcefeed alfalfa gruel, propylene glycol.


Outline strategies for prevention of PEM and Pregnancy Toxaemia in beef cattle.

- Nutrient requirements inc greatly for beef cattle in third trimester of pregnancy.
- Have adequate body condition (5-7/9) entering third trimester and feed adequate amounts of good to excellent quality forage.
- As quality of forage dec, time spent in rumen inc, therefore maximum daily intake of feed dec, therefore feed good quality forage.
- Decreasing temperature inc energy needs e.g. 10 C --> 10% higher energy req, 0 C --> 20% higher energy req.


Ketosis occurs in ruminants during times of increased mobilisation of fat stores, usually just after parturition. List the three ketone bodies which are elevated in the blood of ruminants during ketosis.

- Acetone (Ac).
- Acetoacetic acid (AcAc).
- Beta-hydroxybutyric acid (BHB).


Define type I ketosis.

- Aka classic 'primary' or 'spontaneous' ketosis.
- Causes reduction in glucose in the blood and liver.
- Increased fat mobilisation culminating in elevated ketone body accum from a neg energy balance during early lactation.
- Becomes a dz condition when absorption and prod of ketone bodies exceed their use by the ruminant as an energy source --> elevated blood ketones, NEFAs and dec blood glucose.


Define type II ketosis.

- Involves high blood insulin conc and transient hyperglycaemia secondary to overconditioning and fatty infiltration of the liver.


Describe the aetiology of ketosis in dairy cattle.

- Processes that require glucose peak in late gestation and early lactation; daily glucose req inc 30% in late lactation and 25% w onset of lactation.
- Gluconeogensis must occur for cattle to meet glucose demands; substrate = propionic acid (FFA) which is prod in the rumen or by breakdown of body proteins.
- Alternate energy sources = ketone bodies or fat-derived NEFAs.
- High milk prod in early lactation exceeds ability of cow to ingest sufficient feed to meet this requirement for energy; milk prod peaks at 4wks post-calving, feed intake peaks at 7-8 wk post-calving.
- Cow mobilises body fat and protein stores for gluconeogenesis --> normal dairy cows have some degree of ketone body prod during this time, certain factors tip them over into subclinical or clinical ketosis.


List risk factors for development of subclinical or clinical ketosis in dairy cattle.

- Any dz that dec feed intake: mastitis, metritis, peritonitis, LDA most common; subclinical hypoCa, mild ruminal overload, laminitis, lameness, pyelonephritis and musculoskeletal calving inj less common.
- Poor quality/low energy feed.
- Ingestion of pre-formed ketones e.g. in ketogenic silage.
- Cobalt deficiency.
- Concentrates with low levels of lincomycin have been reported in herd outbreaks of ketosis.


List clinical signs of clinical ketosis in dairy cattle.

- Gradual loss of appetite and dec in milk production over several days.
- Rapid weight loss.
- Type I: typically 3-6wks post-partum.
- Type II: typically immediately post-partum.
- Normal TPR.
- Firm, dry faeces.
- Moderate depression.
- +/- reluctance to move.
- Ruminal atony if inappetent for several days.
- +/- pica.
- +/- odour of ketones on breath and in milk.
- +/- transient nervous signs e.g. staggering, blindness.
- +/- primary dz: mastitis, metritis, peritonitis, LDA (NB ketosis inc risk of LDA so may be primary or secondary).


List clinical signs of nervous ketosis in cattle.

- Acute onset of bizarre neuro signs lasting 1-2h and recurring at 8-10h intervals.
- Circling, proprioceptive deficits, head pressing, apparent blindness, wandering, excessive grooming, pica, ptyalism.
- +/- hyperaesthesia, bellowing, moderate tremors, tetany.
- +/- aggression towards people of inanimate objects.
- +/- ataxia when walking.


List clinicopathologic abnormalities in cattle with ketosis.

- Detection of ketone bodies in plasma, milk, urine.
- Blood glucose conc 20-40 mg/dL.
- Total blood ketones > 30 mg/dL.
- Total urine ketones > 84 mg/dL (better indicator than blood ketones).
- Total milk ketones > 10 mg/dL.
- Blood BHB > 3 mmol/L.
- AST, SDH elevated in severe cases.
- Plasma insulin elevated initially then depressed w anorexia.
- Subclinical ketosis: no Csx but low-normal blood glucose, blood ketones 10-30 mg/dL, milk ketones 2 mg/dL, BHB 1.2-2.9 mmol/L, blood NEFAs > 0.5 mEq/L.


What factors mainly influence the control of blood glucose in ruminants?

- Insulin.
- Favours cellular uptake of glucose, lipogenesis, glycogen synthesis.
- Decreases lipolysis and hepatic gluconeogenesis.
- Ruminants are relatively insulin resistant, but during early lactation low insulin conc are accomp by high tissue insulin sensitivity.


Describe the effects of glucagon, catecholamines and growth hormone on glucose control in the cow.

- Glucagon: counteracts insulin by inc lipolysis and hepatic gluconeogensis and dec lipogensis.
- Catecholamines: favour lipolysis and dec lipogensis.
- GH: high in early lactation; inhibit lipogensis, inc gluconeogensis.


Adipose tissue acts as an endocrine organ. Do adipose tissue hormones play a role in energy balance in cattle?

- Leptin: influences feed intake and resistance to insulin and inc energy expenditure.
- Leptin is elevated in people w obesity.
- Role unknown in ruminants.


List the three main VFAs produced in the rumen of cattle and their subsequent metabolism.

- Acetate, propionate, butyrate; 70:20:10 ratio.
- Acetate: mainly used in fat synth
- Butyrate: condensed into acetoacetyl CoA --> oxidised to ketone bodies or --> acetyl CoA --> TCA cycle (no net gain of glucose).
- Propionate: enters TCA cycle at levels of succinyl CoA --> 30-50% glucose production in the ruminants.
- Acetate and butyrate are ketogenic, propionate is glycogenic.


In what organs are ketone bodies produced in the ruminant and what organs use them as an energy source?

- Produced in ruminal epithelium, mammary gland, liver.
- Used by TCA cycle in heart, kidney, skeletal muscles, mammary gland.


Describe oxidation of acetyl CoA in lactating cattle.

- Efficient oxidation of acetyl CoA depends on supply of oxaloacetate (generate from propionate, lactate and pyruvate).
- Lactating cow diverts proprionate and lactate to milk to produce lactose --> dec supplies of oxaloacetate.
- Backlog of Acetyl CoA is unable to enter TCA cycle and is diverted into the formation of ketone bodies.


Describe metabolism of adipose tissue as an energy source in ruminants.

- Adipose tissue stores energy in the form of TGs.
- TGs are mobilised to form NEFAs.
- NEFAs enter TCA cycle through acetyl CoA (--> more ketone bodies) or are re-esterified into triglycerides/ triaglyceride (TAG).
- Ruminant liver is inefficient in partitioning NEFAs into TGs and secreting them into circ as VLDLs; apoprotein B is req to form VLDL so defic --> accum of TAG/fatty infiltration of the liver + elevated ketone bodies.
- Ketone bodies in clinical ketosis are mainly prod from NEFAs in the liver, which shift in response to low carb supplies from pathways of esterification and complete oxidation of acetyl CoA to CO2 to partial oxidation of acetoacetyl CoA to ketone bodies.


Describe negative consequences of subclinical ketosis in dairy herds.

- Cattle with BHB > 1.2mmol/L by 3-5 days in milk were 6.6 x more likely to develop DAs, 4.5 x more likely to be removed from the herd, prod 2.2 kg less milk/day during first 30d in milk.
- Cows as higher range of BHB > 2.4 mmol/L were 3 x more likely to dev DAs, 50 x more likely to be removed from the herd, prod 180 kg less milk during first 30d in milk.


Describe factors of signalment which increase the incidence of clinical ketosis in dairy cattle.

- Incidence increases w parity; peaks at 5th-6th lactation.
- Cows dx w clinical ketosis once are more likely to develop it again at subsequent calvings.
- High producers.
- Cows that are over-conditioned at calving.


Describe environmental and dietary factors associated with increased incidence of clinical ketosis in dairy cattle.

- Season (inc incidence during mid-winter).
- Climate.
- Stabling (inc in stables vs loose housing).
- Feeding (inc w greater number of feedstuff and dec feedings per day).
- Diets


Describe necropsy findings in cattle with ketosis.

- Mortality with primary ketosis is very low; fatty liver is only finding.
- In animals with secondary ketosis findings will be related to the primary condition e.g. metritis, peritonitis.


Outline treatment of clinical ketosis in dairy cattle.

- Goal of Tx: limit mobilisation of fat by increasing availability of glucose or glucose precursors and promoting uptake of glucose by cells.
- Oral propylene glycol is treatment of choice.
- If nervous ketosis Tx w IV 50% dextrose.
- Use of insulin rarely required unless refractory cases or if hepatic lipidosis has occurred.
- Use of corticosteroid is not recommended but was traditionally used to dec tissue uptake of glucose and reduce milk production.
- Tx of secondary ketosis requires correction of primary condition while ensuring provision of an adequate diet.
- NB in a study w IV boluses of 50% glucose --> rapid dec in blood ketones and NEFAs and impr in CSx BUT return to pre-tx levels w/in 12h therefore in hospital scenario CRI of 2.5% glucose preferred until urine ketones have dec.


Oral propylene glycol boluses (8-10oz) can be used to tx clinical and subclinical ketosis. Describe the mechanism of action of propylene glycol in resolving ketosis.

- Increases supply of gluconeogenic precursors (propylene, propionate and propranolol) to the liver.
- Decreases the glucose demand by peripheral tissues.
- Blood glucose rises and induces insulin release.
- Insulin release slows release of TGs from adipose tissue and therefore dec prod of NEFAs and BHB.


List deleterious effects of propylene glycol overdose in cattle.

- Deleterious effect on rumen microflora.
- Decreased ruminal motility.
- Diarrhoea.
- Tx by discontinuing propylene glycol and transfaunating cow.


List dietary supplements that can be given to cows with ketosis and their mechanism of action.

- Glucose precursors: gylcerol, sodium propionate, ammonium lactate, sodium lactate.
- Lipotrophic agents (inc mobilisation of fat in the liver and prod of VLDLs): choline, l-methionine.
- Cobalt (precursor of vit B12) or vit B12, which is essential co-factor in metabolism of priopionate as it enters the TCA.
- Chromium: may potentiate action of insulin.
- Nicotinic acid (niacin) and nicotinamide: dec blood ketones and FFAs and inc blood glucose.
- Ionophores: inc ration of propionate formation in the rumen and decrease incidence of clinical ketosis.


Outline methods for prevention of clinical ketosis in dairy cattle.

- Feeding during late lactation and the dry period should promote good body condition at calving.
- Introduce lactating ration in a stepwise fashion to promote optimum intake at commencement of lactation; commence at 4-5wks pre-calving and inc to ad lib levels at 2-4wks of lactation.
- Key aspects of ration: high energy density, optimum levels of protein and fibre, balanced in minerals.
- Substitution or dilution of ketogenic silage for cattle in early lactation.
- Early detection: test milk or urine for ketone bodies for first 2-8wks post-calving.


What proportion of dairy cows experience subclinical hypocalcaemia (

- 50% of dairy cattle.
- Reduced ruminal and abomasal contractility.
- Reduced feed intake.
- Increased blood NEFA concentrations.
- Can contribute to dev of several clinical conditions: mastitis, metritis, retained placenta (dec uterine and teat sphincter contractility).
- Dec ability of immune cells to respond to external stimuli.


Describe clinical signs of periparturient hypocalcaemia (Milk Fever) in cattle.

- Ataxia.
- Mild bloat (eructation is reduced).
- May become recumbent and be unable to rise.
- Lie w neck in S-shaped curve.
- Muscle fasiculations.
- Heart sounds muffled due to dec contractility.
- Tachycardia to compensate for low ventricular ejection volumes.
- Loss of ability to thermoregulate --> hypo/hyperthermia.
- CSx occur just before calving to 2 days after calving due to rush of Ca into mammary gland to form colostrum.
- Also occur with many infectious conditions, especially if endotoxins are elaborated e.g. mastitis, metritis.


List the three main electrolyte imbalances which result in Downer Cow Syndrome.

- Hypocalcaemia: plasma Ca


Outline treatment of Milk Fever in cattle.

- IV calcium; commonly in form of calcium borogluconate +/- Mg, P, gluc; ideal dose = 2g/100kg BWt.
- Administer Ca at rate of 1g/min; too rapid admin --> fatal arrhythmia.
- IV Ca typically raises blood Ca for 4h post inj.
- Can supplement with SC or IM inj or oral Ca salts to help prevent relapses 12-24h post IV admin.


Describe the role of PTH in Milk Fever in diary cows and the influence of diet on the efficacy of PTH.

- Initially thought high Ca diet pre-calving --> positive Ca balance --> PT gland atrophy --> lack of PTH in response to hypoCa of lactation.
- This is now disproved as PTH is WNL or high --> efficacy of secreted PTH is poor and fail to inc blood Ca conc.
- Metabolic alkalosis alters conformation of PTH receptor rendering tissues less sensitive to PTH.
- Metabolic alkalosis occurs in dairy cows fed high K+ diets.
- Using a DCAD method to create a diet which induces compensated metabolic acidosis prior to calving --> PTH receptor is best able to response to PTH secreted at onset of calving.
- Anions e.g. Cl-, SO4- should be added to diet until --> urine pH 6.2-6.8 Hoslteins, 5.8-6.3 Jerseys.
- High P diet --> high blood P --> inhibits activity of renal 25-hydroxyvitamin D 1a-hydroxylase enzyme --> dec renal resorption of Ca and dec intestinal absorption of Ca; diet should be 30-40g P/day.
- HypoMg also prevents action of PTH on tissues and inhibits PTH secretion; feed 0.4% Mg pre-partum and during early lactation.
- Feed low-Ca diet during late gestation to stimulate activity of osteoclasts and enterocytes in preparation for lactation and then at calving and 24h later give 50-125g oral Ca.


Describe the mechanism by which hypocalcaemia occurs in late gestation beef cattle and ewes.

- Esp if carrying twins sudden inc in foetal skeletal demand for Ca is greater challenge than lactation.
- Estrogen inc in late gestation --> dec osteoclastic activity.
- Inadequate Mg intake also often contributes.
- Can be prevented by inc Ca and Mg content of diet during gestation for beef cattle and ewes.


Describe the role of magnesium in normal homoestasis in cattle and how plasma magnesium concentrations are maintained.

- Major intracellular cation; serves as co-factor for enzymatic reaction vital to every major metabolic pathways.
- Vital for normal nerve conduction, muscle function and bone mineral formation.
- Plasma Mg is nearly entirely dependant on continuous dietary Mg absorption.


List clinical signs of hypomagnesaemia in cattle.

- Excitability.
- Tetany.
- Convulsions - chomping jaws, frothy salivation; liew w head arched back and legs paddling.
- HR up to 150bpm w very loud heart beat.
- RR up to 60pm.
- Hyperthermia due to muscle activity.
- Sudden death.
- Moderate hypoMg (1.1-1.8 mg/dL) --> reduced feed intake, nervousness, reduced milk fat and total milk prod.


Outline the role the rumen and dietary influences play in hypomagnesaemia in cattle.

- Calves/lambs: SI site of Mg absoprtion.
- Adult ruminants: rumen and reticulum site of Mg absorption, SI site of Mg secretion.
- Rumen Mg absorption depends on amount of Mg in solution and Na-linked active transport process.
- Low soluble Mg conc in rumen occurs w low dietary Mg content of forages, inadequate dietary Mg supplementation, rumen pH > 6.5, certain organic compounds in forage e.g. UFAs --> insoluble Mg.
- Rumen pH typically high in grazing animals due to salivary buffer secretion; high-grain ration --> rumen pH greater Mg absorption.
- High dietary K depolarises apical membrane of ruminal epi --> less transport of Mg across epi.
- Feeding ionophore impr activity of Na-linked Mg trans.
- Lush pastures --> inc GI transit time --> insufficient time of Mg in rumen for absorption.


Describe risk factors for development of hypomagnesaemia in ruminants.

- Beef cows, dairy cows and ewes in early lactation grazing lush pastures high in K and N and low in Mg and Na; known as grass/lactation/spring tetany, grass staggers.
- Occurs in Spring and Autumn --> cool weather, pasture growing at maximal rates.
- Ewes are generally hypoCa and hypoMg in 2nd-4th wk of lactation, suckling more than 1 lamb.


Describe clincopathologic findings in cattle with hypomagnesaemic tetany.

- CSx due to CSF Mg


Outline treatment of hypomagnesaemia in ruminants.

- Tx ASAP; response often disappointing; directly related to time elapsed b/w onset of CSx and Tx.
- 1.5-2.25g Mg/adult cow; come in IV solutions as chloride, borogluconate or hypophosphite salts.
- Cows should not be stimulated to rise for at least 30mins post Tx as may precipitate further tetany.
- Cows that do recover usually do so within 1h of Tx (time taken for CSF levels to inc); often relapse w/in 12h.
- Reduce risk of relapse by drenching w Mg oxide +/- Ca, P, NaCl slurry.
- Immediately administer Mg to remainder of herd in grain ration or on hay/pasture.


Outline methods of prevention of hypomagnesaemic tetany in cattle.

- Ensure ruminal Mg content high enough that it will flow down conc gradient into ECF if active absorption mechanism is impaired --> 0.35-0.4% Mg in close-up rations.
- Blood sample w/in 12h of calving; if serum Mg is not at least 2 mg/dL in 9/10 cows samples inadequate dietary Mg absorption can be presumed.


Describe the main features of phosphorus metabolism in cattle.

- ECF P pool maintained by replacing P removed for bone and muscle growth, endogenous faecal loss, urinary loss and milk prod and dietary P abs or resorption from bone.
- Salivary secretions remove large vol of P from ECF pool; influenced by time spent ruminating and PTH; imp to buffer rumen; most reabsorbed in SI but also lost in urine.
- Phytate-bound P in plants is absorbed in SI following digestion of phytic acid by ruminal microbes; P absorbed in excess of need --> excreted in saliva and urine.
- PTH inc renal and salivary P excretion, therefore hypoCa animals often become hypoP.


Describe the consequence of chronic hypophosphataemia due to diet marginal in P in late-term pregnant ruminants.

- Chronic hypoP becomes pathologic during late pregnancy as P requirement of foetus accelerate.
- Animals become recumbent.
- Appear alert and will eat food put in front of them but are unable to rise.
- Often have concurrent hypoCa, hypoMg, hypoglycaemia (low P often = low energy diet as grain is high in P).


Describe hypophophataemia in cows with Milk Fever.

- P normally dec at onset of lactation due to diversion of P from extracellular pool to milk and colostrum.
- If animal also has hypoCa --> PTH secretion --> further hypoP due to loss in urine and saliva.
- Plasma P conc usually rise rapidly following Tx for hypoCa with IV Ca and resultant dec in PTH secretion.


Define Hypophosphataemic Downer Cows.

- Cows with Milk Fever in which plasma P does not increase in response to administration of Ca; plasma P


Outline treatment of Hypophosphataemic Downer Cows.

- Tx can affect recovery in some animals if admin prior to muscle and nerve damage from recumbency.
- 50g oral P in form of 200g monosodium phosphate or 6g P IV in form of 23g monosodium phosphate in 1L saline.
- NB P in 4-in-one products useless as biologically inactive (phosphite or phosphinic acid).


Describe the clinical presentation of chronic phosphorus deficiency due to poor soil P quality in ruminants.

- Occurs in arid or tropical climates.
- Infertility NB due to poor energy in pasture not P defic.
- Poor growth rates.
- Rickets.
- Osteomalacia.
- Unthrifty appearance.
- Reduced feet intake or pica.
- Reduced milk production.


Describe the lesion which occurs in rickets. How is this different to osteomalacia?

- Occurs in young, growing animals in which the cartilaginous matrix at the growth plate and the osteoid matrix formed during bone remodelling fail to mineralise.
- Osteomalacia occurs in adults and is solely failure of osteoid matrix to mineralise.


Describe the aetiology of rickets and osteomalacia in cattle.

- Dietary P deficiency.
- Can also occur with vitamin D deficiency; common to see mixed lesions of Ca and P deficiency w vit D deficiency, but rickets/osteodystrophy predominate.
- NB different from Ca deficiency --> normal osteoid is not formed at all (osteoporosis) or is replaced by fibrous material (osteodystrophy).


Describe the syndrome of Post-parturient Haemoglobinuria in cattle.

- Intravascular haemolysis, anaemia and haemoglobinuria during the first 6 weeks of lactation.
- Many, but not all, cattle are hypophosphataemic.
- Inc risk in cattle that were Tx for ketosis.


Describe the proposed pathogensis of Post-parturient Haemoglobinuria in cattle.

- Severe hypoP --> depressed ability of RBCs to prod ATP --> insufficient ATP to power Na pumps --> inc intracellular Na --> rigid RBCs that rupture as they pass through capillary beds.
- HypoP alone rarely sufficiency to cause inc RBC fragility.
- Often cows also on diet low in Se, Cu and energy, so likely combination of factors, not just hypoP.


Define Hypokalaemia Syndrome in cattle.

Presence of flaccid paralysis, recumbency, abnormal neck position and serum K conc


Describe signalment of cattle that develop Hypokalaemic Syndrome.

- HypoK commonly occurs w anorexia and GI stasis.
- Hypokaelaemic Syndrome is rarely reported (42 cases in the literature).
- Reported most commonly in lactating dairy cows


List risk factors for development of Hypokalaemic Syndrome in cattle.

- Recent administration of isofluprednone.
- Multiple doses of dextrose and insulin.
- 2 calves: IVFT 2+ days w/out serum biochem.
- Other initiating dz e.g. acetonaemia or infectious dz.


Describe clinical signs of Hypokalaemic Syndrome in cattle.

- Early stages: absence of faeces, paretic gait, hyphosis, inability to stand for a long time, tachycardia.
- May see abnormal neck posture.
- Typical presentation: recumbency, S-shaped neck, abnormal faeces and ruminal motility, abnormal appetite (will eat if brought to them), tachychardia +/- arrhythmia.
- Flaccid paralysis: recumbency, little or no tail tone, unable to raise head, as soon as released moves back to S-shaped neck.
- Arrhythmias: VT, accelerated escape ventricular rhythm, atrial fibrillation, flattened T waves.


Describe the aetiology of Hypokalaemic Syndrome in cattle.

- Imbalance of internal (EC-IC) or external (intake vs loss) K balance or both.
- Exact determinate unknown, except for in cases of isofluprednone administration.
- Isofluprednone ---> inc renal loss due to mineralocorticoid activity.
- Severe dz --> K depletion through anorexia, catecholamine release, urine loss (failure to adapt from high K diet to sudden lack of intake).


Outline methods to diagnose Hypokalaemic Syndrome in cattle.

- Pathognomonic CSx of twisted, S-shaped neck associated with flaccid paralysis.
- Serum K


Describe treatment of Hypokalaemic Syndrome in cattle.

- Oral KCl supplementation (only oral + IV if dehydrated, otherwise IVF --> inc K diuresis): total 60-100g/100Kg/d.
- Nursing care essential to prevent complications of recumbency e.g. mastitis, myopathy.
- Serum K normalises in 3d; some degree of paresis may continue for a further 1-2d.
- Supplement K for 1-2d afte return to normal appetite and clinical state, slowly dec to avoid K depletion caused by delayed renal adaptation to lower K diet.