13/10/14 Flashcards

1
Q

Krebs cycle end product

A

ATP i.e. energy NOT glucose

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2
Q

Rumen breaks glucose down into

A

c3 molecules. ++++c3 will lead to acidosis

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3
Q

How does Ketosis come about (with ref to c3 molecules)

A

Insufficient energy i.e. insufficient glucose–> insufficient c3 (broken down by rumen) therefore accumulation of acyl-CoA = FATS/KETONES

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4
Q

Effects of raised Ketones

A

Raised Ketones reduce appetite further reducing the supply of c3 molecules therefore further build up of acyl-CoA = vicious circle known as the Ketosis complex. COW’S DON’T DEVELOP KETOACIDOSIS = CATS

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5
Q

All cows post partum will have

A

+ ve ketone result = normal degree of fat mobilisation.

Ketosis complex: 2-10 weeks after calving

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6
Q

Ketosis complex higher risk examples

A

2-10 weeks after calving

Hypocalcaemia, hypomag, RFM, lameness, twin carrying cows ALL AT HIGHER RISK

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7
Q

Primary Ketosis vs Secondary Ketosis

A

Primary Ketosis: Voluntary feed intake cannot meet energy demands. Excessive breakdown of body fat and muscle. Sometimes due to specific nutrional deficiencies. aka starvation ketosis. Enough space? Stale food??
SECONDAR ketosis: Any condition that makes cow loose appetite LDA/RDA, Metritis, Mastitis

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8
Q

Ketosis Wasting form vs Neurological form

A

Wasting form: Gradual reduction in appetite, cows refuse to eat concentrates, marks loss of body weight, firm dry faces.
Neurological form: Sudden onset of abnormal behaviour; walk in circles, depreaved appetite, hyperaesthesia.

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9
Q

Clinical signs of Ketosis

A

Blood gluc = low end
Blood beta-hydroxbutyrate (BHBA)
Milk and Urine Ketone levels
Serum NEFAs can be elevated

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10
Q

Ketosis treatment

A

IV Dextrose, quick
IV Dextrose 200g slow
Corticosteroids (app stimulant) NOT IN PREGNANT!
Propylene glycol (c3 molecule precursors)

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11
Q

Pregnancy Toxeemia in cattle

A

Primarily a disease of beef cattle
Seen more in autumn calving
IF shortly before calving = agitated, incoordinated, difficulty rising, scant faces
WHEN 6 weeks before calving, depressed

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12
Q

Preg toxaemia in sheep presentation

A

Affected ewes separate from flock, apparently blind.
Constipation common and griding of teeth.
Periods of drowsiness and stargazing +- in coordination
Ewes recumbent
CHECK ALIVE

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13
Q

Diagnosis of FLS and preg tox

A

Blood NEFAs, glycose, liever enzymes

Milk fat > 5% Protein 5% fat

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14
Q

Treatment of FLSa and preg tox

A

As for ketosis (dextrose IV, propylene glycol?) but consider insulin, steroids, high quality feed.
Drench every 4-6 hours
Early stages could induce preg/ caesarean.
Affected flocks IMMEDIATELY placed on supplementary feeding

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15
Q

Defintion of Down Cow

A

A cow that is down for >24 hours of after unsuccessful treatment for Ca, Mg, P

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16
Q

Down cow problem

A

Primary cause may be resolved but secondary superficial nerve damage or ischemic necrosis of muscle (esp hind limb)
Compression–> anoxia–> cell damage –> inflamm –> further swelling –> poor tissue perfusion

17
Q

Peroneal nerve damage

A

Cause hyperflexion of the fetlock (knuckled)

18
Q

‘Happy’ downer or creeper cows think…

A

Phosphorous deficiency

19
Q

Full clinical examination

A
Check for broken legs
Check for ruptured cruciates
Check for dislocated joints
Check for neurological function
Check uterus, pelvis and peritoneum 
CHECK ALL QUARTERS OF UDDER --> Check if toxic
20
Q

Care of the downer cow, leg positioning

A

Sit cow up, sternal recumbancy.
Get the legs underneath to reduce further ischaemia due to pressure on limbs.
Rotate cow every 4-6 hours
Hobble

21
Q

Prognosis

A

Cow raising body on all 4 but missing force: reserved optimism, shows nerves are working
If no progress after 48 hours: euthanasia.
Down for 3 days, chances of recovery= 20%