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Cattle > metabolic disease in cattle > Flashcards

metabolic disease in cattle Flashcards

1
Q

Type 1 vs type 2 ketosis

A

Type 1: around peak lactation i.e 6-8 weeks post-calving

Type 2: much earlier; within 2 weeks of calving

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2
Q

Basic pathophysiology of ketosis

A

Negative energy balance leads to intense adipose mobilisation + high glucose demand
- Liver produces ketones as it breaks down fat

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3
Q

Consequences of negative energy balance ketosis

A

Adipose mobilisation –> excess NEFAs (toxic) –> incomplete oxidation due to insufficient hepatic metabolism –> ketone bodies mainly BHB
Increased fat storage in the liver

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4
Q

When is the critical period in risk of ketosis

A

End of dry period i.e just before calving
BECAUSE DMI decreases by 20% due to fetus squashing rumen
+ change in energy metabolism as birth/lactation approaches

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5
Q

What does increased fat storage in liver (from -ve energy balance lead to)

A

Impaired gluconeogenic capacity
- Subclinical ketosis
- Chronic fat modbilisatio = fat fatty liver syndrome
- Massive accumulation of lipid in obese cows = fat cow syndrome
Fat infiltration of liver reduced hepatic macrophage (Kupffer cell) function so predisposition to sepsis

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6
Q

Signs of primary ketosis (i.e not due to other condition stopping them eating

A

Reduction in rumen fill
Smell of ketones on breath, urine, milk
Drier manure
Dry coat and piloerection
Neurological signs = nervous ketosis
Recumbency
ataxia

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7
Q

Which primary diseases are commonly responsible for secondary ketosis

A

LDA; get slow GI transit
Metritis: toxaemia puts animal off food

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8
Q

Signs of subclinical ketosis

A

Elevated BHB levels, reduced production, decreased appetite

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9
Q

What is fat cow syndrome

A

Severe hepatic lipidosis
From cows too fat before parturition; eat less so quickly swing into -ve energy balance
- More quickly get hepatic lipidosis because more fat available to be mobilised

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10
Q

What life threatening condition do we usually see alongside fat cow syndrome

A

Hypocalcaemia

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11
Q

What is pregnancy toxaemia

A

When cows in late pregnancy develop ketosis; often relates to multiple fetuses, inappropriate diet or restriction of intake, other illnesses

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12
Q

What does a urine dipstick for ketosis measure

A

Acetoacetate as proxy for BHB (BHB not excreted in urine)

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13
Q

What is Rothera’s reagent a crude test for

A

Ketosis

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14
Q

What level of BHB concentration give subclinical and clinical ketosis

A

Subclinical = >1.4mmol/l
Clinical = >3mmol/l

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15
Q

How can we diagnose hepatic lipidosis

A

Biochemistry can show hepatic damage/dysfunction: high AST, GGT, SHD
Liver biopsy shows fat levels; normal liver is <13%; clinical disease is >25%

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16
Q

Treating pregnancy toxaemia

A

= EMERGENCY to prevent irreversible hepatic lipidosis and organ failure
- Intensive support; glucose therapy, force feeding
- May need to induce parturition or C section to get fetus energy drain out

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17
Q

Treating ketosis

A

Give IV glucose (50% - 400ml)
ALso corticosteroids to reduce milk yield (demand for energy) + stimulate appetite and gluconeogenesis
Propylene glycol –> converted to oxaloacetate as precursor for gluconeogenesis (BUT need functioning liver for this to work)
Proprionate = direct gluconeogenesis precursor

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18
Q

What might vague sick cows in early lactation have

A

Hepatic lipidosis

19
Q

How do ionophore boluses e.g monensin help prevent ketosis

A

Alter ruminal microflora to decrease acetate production and increase proprinoate production

20
Q

What NEFA level do we want (when taken 10 days post calving) so be unlikely to get ketosis

A

<0.5mmol/l

21
Q

When do we consider a herd to have. problem with ketosis

A

When >20% have a BHB concentration of >1.4 mmol/l ie subclinical ketosis

22
Q

How much Ca2+ is needed per day in a cow; and how much at full term pregnant; and how much at lactation

A

25g normally
39g full term
100g lactation (max)

23
Q

What does hypocalcaemia cause to muscles

A

Flaccid paralysis

24
Q

is hypocalcaemia an issue of hormones or dietary intake

A

Hormones; failure to respond to PTH

25
Q

effect of oestrogen on Ca2+ mobilisation

A

negative

26
Q

3 stages of hypocalcaemia

A

1) Cow still after to stnd
2) Recumbency
3) Coma

27
Q

What finally causes death following hypocalcaemia

A

bloat

28
Q

What do we give to the hypocalcaemic cow

A

Need to give at least 8g calcium
- Bottles are 400ml of either 40% (13g) or 20% (6.8g) CBG (calcium borogluconate)

Probably give one subcut while down and one IV (expect cow to get up quickly after IV)

29
Q

Subclinical hypocalcaemia effects

A

Sluggish GI tract movement; can predispose to LDA
Poor uterine involution; predisposes to RFM
Teat sphincter may not close properly; mastitis risk

30
Q

What decreases body response to PTH

A

MEtabolic alkalosis
Hypomagnesia (receptor needs this to work)

31
Q

Why and how might we want to make levels of Ca2+ in late gestation low

A

TO ramp up system to supply Ca2+; increase exposure of system to PTH to overcome negative effects of alkalinisation

  • Can use Ca2+ binders
32
Q

What might we want to acheive via cation-anion dietary changes in late gestation to avoid hypocalcaemia

A

Metabolic acidosis (because alkalosis decreases response to PTH)
- Dry cow diet is between -100 and -250 mEq/kg

33
Q

What are creeper cows

A

Recumbent that don’t respond to Ca2+ and push around on sternum
= from hypophosphataemia

34
Q

What causes hypophosphataemia

A

Usually excess calcium, iron, aluminium
- Can be from low intake

35
Q

What causes hypokalaemia

A

Usually secondary to low
- To ICF in metabolic alkalosis
- Increased loss in urine e.g in anorexia or corticosteroids
Loss from digestive tract in diarrhoea

36
Q

WHat are muscle fasciculation associated with

A

Hypokalaemia

37
Q

WHat is the cause of grass staggers and who do we typically see it in

A

Hypomagnesaemia
Seen in lactating beef suckler cows; 2 months post-calving

38
Q

Why is it so important to have high intake of magensium

A

Only 0.5g in blood/stored
Only 20% absorbed of intake
Most lost in urine/milk

Should intake 30g/day

39
Q

What plants present hypomagnesaemia risk

A

Rye and fast growing leys: low levels
Spring grass: because low in Na+ (needed for Mg2+ uptake) and hgih in K+ (interferes with this) + has high fat which can form insoluble soap with Mg; also low fibre time which can increase gut transit time and reduce Mg absorption

40
Q

How does stress impact hypomagensia

A

Adrenaline causes shift out of blood

41
Q

Signs of acute hypomagnesaemia

A

Early: anoeria, separation, muscle fascilation; vague neurological signs
Later: recumbency, convulsions, death during episode

42
Q

How do we give magnesium to cows

A

SUBCUT
(IV will kill the animal)

43
Q

Signs of subclinical hypomagnesaemia

A

Dullness, low appetite, odd facial expression, behaviour hchanges, low production, unthriftiness

44
Q

How does excess ammonia affect Mg absorption

A

decreases it

Cattle (20 decks)

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