Misc Flashcards

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1
Q

What are the 2 main consequences of NEB in the periparturient cows?

A

Ketosis
Fat mobilisation syndrome
NEB can be 1ry or 2ry

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2
Q

Why has selecting for increased milk yield led to incr susceptibility to NEB?

A

Early lactation- glucose insufficient. Glucose goes to udder independent of insulin control, therefore drains the cows glucose.

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3
Q

What is the ketosis complex?

A

Excessive build up of ketone bodies due to accumulation of acetyl-coA due to lack of C3 molecules. Reduces appetite- vicious cycle. Happens post partum 2-10wks after calving

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4
Q

What causes primary ketosis?

A

Vol feed intake can’t meet energy demands. Excessive breakdown of body fat and muscle.

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5
Q

What causes secondary ketosis?

A

Any condition that makes cows lose appetite. E.g. LDA/RDA, (endo)metritis, lameness, (mastitis)

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6
Q

What is the ketosis wasting form?

A

Gradual reduction in appetite, refuses to eat concentrates, marked loss of body wt, firm dry faeces, occasional transient bolus of staggering.

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7
Q

What is the ketosis neurological form?

A

Sudden onset of abnormal behaviour. Walks in circles, aimless wandering, head pushing, apparent blindness. Develop depraved appetite, licking of skin and objects, chewing. Hyperaesthesia, incoordinated gait. About 10% of ketosis cases.

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8
Q

How is ketosis in cows diagnosed?

A

Clinical signs. Blood glucose (low end). Blood beta-hydroxybutyrate >1.4 subclinical >2.5mmol/l clinical. Milk and urine ketone levels. Serum NEFAs can bee elevated

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9
Q

What is the treatment for ketosis?

A

IV dextrose 100g quick or 200g slow. Corticosteroids. Appetite stimulants. Propylene glycol 250ml bid (rich in C3 molecules) until cow fights you off.

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10
Q

What is fatty liver syndrome?

A

Excessive weight loss. Fat mobilised as NEFA (due to low glucose), deposited in liver. Typically BCS >4 if early on, or was BCS 4 2wks ago but now 2- skinny. Inappetence to anorexia. May become recumbent, get neuro signs and die. Often concurrent condition e.g. RFM or (endo)metritis that doesn’t respond to tx.

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11
Q

What is pregnancy toxaemia?

A

Similar to FLS but presented at a diff stage and typically in diff animal. Last few weeks of gestation, prevalent around parturition, twins. Reduced feed intake 1ry cause, fat animals at risk (lots to mobilise)

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12
Q

How does pregnancy toxaemia present in cattle?

A

Typically beef. More common in autumn calving. Internal parasitism may incr risk.. When shortly before calving, cows/heifer agitated, incoordinated, difficulty rising, scant faeces. When +/- 6 weeks before calving tend to be depressed.

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13
Q

How does pregnancy toxaemia present in sheep?

A

Uncommon in maiden ewes. Case fatality about 100% in clinical cases (fat–> kidney, fatal uraemia). Can be outbreaks. May be associated with hypomag and hypocal. Separate themselves, apparently blind, constipation common, grinding teeth, periods of drowsiness and abnormal posture and incoordination. Recumbent, severe deoression, coma. Recovered ewes show wool break

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14
Q

How do you diagnose FLS and pregnancy toxaemia?

A
Blood- NEFA (>0.7mmol/l), glucose (5%, protein 1.6
Liver biopsy (>15% fat)
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15
Q

How is FLS and preg tox treated?

A

Tx as for ketosis combined with IVFT. Consider insulin, steroids, choline, biotin, cobalt amine, BST. High quality feed, glucose precursor rich. Usually poor response to tx- too late

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16
Q

How is FLS and preg tox tx in sheep?

A

Drench every 4-8hr w/ rehydration sol- most effective. In early stages could induce parturition/ CS. Immediately place on supplementary feeding (conc/ cereal grain) and early cases w/ propylene glycol.

17
Q

How do you control/ prevent NEB?

A

Prevent overly fat or poor condition at time of calving. Transition cow ration to reduce concurrent dz. Early lactation cow should be fed a balanced, high energy dense ration. Good quality forage, maize silage.

18
Q

What are the different causes of a down cow?

A

Hypocalcaemia, hypomagnesaemia, hypophophataemia
Per acute toxic mastitiis, metritis, peritonitis
Physical injury HLs (splits, broken/ dislocated hip)
Obstetrical paralysis
Fat cow syyndrome

19
Q

What is the typical downer cow?

A

Down >24hrs, after unsuccessful treatment. Primary cause may be resolved e.g. Ca, Mg, P.
Poss superficial nerve damage. Ischaemic necrosis of muscle due to compression> anoxia> cell damage> inglamm> further swelling> poor tissue perfusion

20
Q

What are the clinical signs of a downer cow?

A

Usually sternal recumbency. Normal eating and drinking if provided. Normal GIT. Some attempt to stand (lift hind quarters). Abnormal position of PLs (nerves).

21
Q

How do you examine a downer cow?

A

Lateral recumbency- check hind legs and exposure udder. Examine one side, roll over sternum to examine the other side. Broken legs, ruptured cruciates, dislocated joints, neuro function, uterus pelvis and peritoneum per rectum, udder. Palpable all 4 limbs, feel crepitates, fractures, dislocations, joint/ligament damage

22
Q

How should you manage the downer cow?

A

Sternal recumbency, rotate cow every 4-6hr, soft bedding, fresh feed and water. Underfloor with grip. Milk bid for comfort and prevention of mastitis. No progress after 48hr- euthanasia.

23
Q

How do you treat the downer cow?

A

Ensure no metabolic ailment- Ca, Mg, P. Toxic cases treat underlying cause. Fractures, ligament tears, dislocations- euthanise. All others- support the cow, reduce ischaemia.
Care, NSAIDs, vit B complex. Lift the cow

24
Q

What are the techniques for lifting the downer cow?

A

Bagshaw hoist- hip lifter attached over tube coxae, assess if trying to use legs, leave to stand w/ hoist attached- give some slack. Often cause traumatic injuries.
Sling- more comfortable, staff/ skill dependent
Water tank- gold standard, lets cow float, beware cows can drown.
Air bag- roll on inflatable bag, inflate, prevent from rolling off