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ENI2 > Farm animal endocrinopathies > Flashcards

Farm animal endocrinopathies Flashcards

Hepatic lipidosis and ketosis

1
Q

What are potential risks as a consequence of subclinical ketosis in a cow?

A
  • Clinical ketosis
  • Retained foetal membranes
  • LDA
  • Lameness
  • Reduced milk quality
  • Decreased fertility
  • Impaired immune function (increased risk of mastitis, metritis)
  • Culling
  • Death
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2
Q

What are the potential outcomes of a negative energy balance in a cow?

A
  • If mild: subclinical ketosis, and increased fat infiltration in the liver
  • If severe: clinical ketosis and fatty liver syndrome
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3
Q

Compare ketosis in farm animals and diabetic ketoacidosis in small animals

A
  • Ketosis is not consequence of diabetes cf. ketoacidosis

- Also different from acidosis/SARA/acute acidosis in cattle

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4
Q

What are risk factors for a cow developing ketosis?

A
  • Long lactation
  • Higher milk production
  • Increased weight before drying off
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5
Q

When are cattle most at risk of ketosis?

A

During early lactation where milk yield increases rapidly, faster than required increase in food intake and be accomodated for

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6
Q

What is ketosis in early lactation called?

A

Type II ketosis

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7
Q

What is ketosis in peak lactation called?

A

Type I ketosis

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8
Q

Which cows are most at risk of type I ketosis?

A

High yielding cows - unable to eat enough to maintain energy

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9
Q

Compare the energy requirement of a normal cow and a lactating cow

A
  • Normal: BWT/10 = MJ of metabolisable energy/day

- Lactating needs an extra 5MJ ME/litre

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10
Q

Describe the normal physiology of fat mobilisation in lactation

A
  • Mobilise fat as normal
  • Lipolysis puts fat into blood as NEFAs
  • In gut, absorbed propionate, moves into liver and provide source of glucose via gluconeogenesis
  • Glucose produced used to oxidise fatty acids
  • Glucose enters tissues, insulin into tissues and milk to drive metabolism and lactose production
  • NEFAs oxidised in liver using glucose from propionate and gluconeogenesis
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11
Q

Describe the pathophysiology of type I ketosis

A
  • Low propionate, less glucose prod, less oxidation of FAs

- Incomplete oxidation of FFAs = ketones, enter blood stream

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12
Q

What is the most common ketone produced in ketosis?

A

Beta-hydroxybutyrate

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13
Q

Describe the pathophysiology of type II ketosis

A
  • Fat cow, more adipose tissue stores, mobilisation of lots of fat at drying off - cannot eat much
  • Excessive mobilisation of fat, increased NEFAs
  • Elevated fat in blood, insufficient glucose to oxidise, accumulation of FFAs in liver = hepatic lipidosis and ketones
  • Further ketones produced due to impaired hepatic function
  • More ketones, more fat mobilised as less energy produced from liver, continues in a cycle
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14
Q

Why are fat cows more at risk of type II ketosis?

A
  • More fat stores to mobilise

- Insulin resistance so less metabolism and less uptake of glucose into milk

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15
Q

How does the blood insulin in a type I ketotic cow differ from that in a type II ketotic cow?

A
  • High in type II

- Low in type I

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16
Q

What are the key interventions for type I and type II ketosis?

A
  • Type I: post-fresh feeding

- Type II: pre-fresh feeding

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17
Q

What are the clinical signs of ketosis in the cow?

A
  • Off food
  • Milk drog
  • Smell of ketones
  • Nervous ketosis possible
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18
Q

What is meant by nervous ketosis? What are the signs? Prognosis?

A
  • Rare presentation of ketosis
  • May be due to hypoglycaemia, ketones, other circulating chemicals
  • Can become aggressive, non-stop forward movement, furious licking
  • Very good prognosis and can recover quickly
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19
Q

What are the clinical signs of hepatic lipidosis in the cow?

A
  • Off food
  • Milk drop
  • Immunosuppression
  • Collapse
  • Liver failure
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20
Q

What is pregnancy toxaemia in sheep and when does it occur?

A
  • Twin lamb disease

- Usually before lambing

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21
Q

Explain the pathophysiology of pregnancy toxaemia in sheep

A

Twins not split from singles, not fed enough, energy demads too high = ketosis

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22
Q

How does pregnancy toxaemia relate to hypocalcaemia

A
  • Clinical signs indistinguishable

- Often one will precipitate the other

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23
Q

What are the clinical signs of pregnancy toxaemia?

A
  • Off feed
  • Dull, depressed
  • Nervous sings e.g blindness
  • Death
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24
Q

What conditions may cause pregnancy toxemia?

A
  • Tooth disease/lameness may pregent eating enough
  • Conjunctivitis (Mycoplasma conjunctivi), often relapse, poor immunity
  • Sporadic cases
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25
Q

What often triggers outbreaks of pregnancy toxaemia?

A
  • Change in management esp. diet

- May lead to reduced DMI

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26
Q

What diagnostic tests should be used in suspected cases of ketosis?

A
  • Blood test for ketones
  • Urine ketone dipstick (small animal/human dipstick)
  • Milk Rotheras’s reagent, turns purple if ketones present, rare
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27
Q

What diagnostic tests should be used in suspected cases of hepatic lipidosis?

A
  • Ketones as with ketosis (blood, urine, milk)
  • Blood NEFAs
  • Evidence of liver damage i..e elevated liver enzymes AST, GGT
  • Assess fat in liver (biopsy, necropsy)
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28
Q

What treatments are available for an individual with hepatic lipidosis, ketosis or pregnancytoxaemia?

A
  • Glucose precursor
  • Glucocorticoid
  • Glucose
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29
Q

Describe the use of glucose precursors in the treatment of hepatic lipidosis/ketosis/pregnancy toxaemia

A
  • E.g. propylene glycol
  • Enters TCA cycles and creates insulin peak
  • Is the base of ketosis treatment
  • 300g once daily
  • Use precursor so rumen flora cannot use it up before it enters blood as would occur with glucose
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30
Q

Describe the use of glucocorticoids in the treatment of hepatic lipidosis/ketosis/pregnancy toxaemia

A
  • Promote gluconeogenesis

- HOWEVER evidence equivocal but still commonly used

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31
Q

Describe the use of glucose in the treatment of hepatic lipidosis/ketosis/pregnancy toxaemia

A
  • Can only be given IV
  • Rapid peak and decline
  • No clear evidence
  • Good for use in nervous ketosis to resolve signs quickly
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32
Q

Compare energy balance disease in camelids with those in ruminants and horses

A
  • Ketosis like a cow
  • Hyperlipaemia like a horse, hepatic lipidosis may occur in extreme cases (usually fatal)
  • Always hyperglycaemia
  • Pregnancy toxaemia may also occur
  • Measure ketones and TAGs
  • Better at dealing with lower energy intake
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33
Q

What are the main risk factors for milk fever?

A
  • Around calving
  • Older cows
  • Diet with a high DCAB
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34
Q

Why is the period around calving a key risk period for milk fever?

A

Ca demand increases rapidly around calving, endocrine control takes a few days to adjust

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35
Q

Why are older cows more at risk of milk fever?

A

Have reduced calcium reserves, and milk fever risk increases with parity

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36
Q

Briefly outline the mechanisms involved in ccalcium metabolism in response to low calcium

A
  • Increased PTH
  • Activates 1-alpha-hydroxylase in the kidney, which activates calcitriol (vit D), which increased resorption in the bone and absorption from the gut
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37
Q

What do all clinical signs of milk fever relate to?

A

Poor muscle contraction

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38
Q

List the clinical signs commonly associated with milk fever

A
  • Constipation, rumenal bloat
  • Skeletal muscle weakness leading to S-bend neck
  • Poor contractility of cardiac muscle leading to slight increased HR
  • GI stasis
  • Poor uterine involution
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39
Q

How can you differentiate between a cow with milk fever and one with toxicity?

A

Milk fever cow has increased HR, whereas a toxic cow has decreased HR

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40
Q

What are the differential diagnoses for a downer cow? How can these be differentiated from milk fever?

A
  • Hypomagnesaemia: thrashing limbs and hyperaesthesia
  • Toxicity, hypovolaemia, sepsis, mastitis: sunken eyes, diarrhoea
  • Non-weight bearing on limb: trauma (NB may be secondary to milk fever causing weakness)
  • Botulism: cows at different stages of lactation affected, tongue protruding from mouth, history of spreading broiler waste on pasture
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41
Q

Describe the appropriate treatment of an individual with milk fever

A
  • Take blood sample prior to calcium administration in case of no response
  • 400ml 40% calcium borogluconate slowly IV
  • Monitor HR and rhythm (risk of dysrhythmia)
42
Q

What are the signs of effective treatment for milk fever?

A
  • Eructation
  • Defaecation
  • Standing
43
Q

What additional treatments can be given to a cow with milk fever?

A
  • Commonly Ca subcut
  • Phosphorous
  • Oral Ca
  • NSAIDs
  • Or no additional treatment
44
Q

Discuss the use of subcut Ca in the treatment of milk fever

A
  • Poor absorption, negative feedback suppression (would normally cause homeostatic mechanism to kick in and stabilise)
  • Little evidence for efficacy
  • Easy and relatively common
45
Q

Outline the use of oral Ca in the treatment of milk fever

A
  • Well absorbed, requires GI uptake
  • Relatively easy
  • Becoming more common
46
Q

Discuss the use of NSAIDs in the treatment of milk fever

A
  • Should be given
  • Cow will have hit the floor hard, trauma likely, pain likely
  • Pain may be preventing cow getting up
47
Q

Discuss the use of phosphorous in the treatment of milk fever

A
  • Often low with milk fever
  • Common preparation used is not active, most is excreted in non-biologically active form in the kidneys
  • Should increase with Ca anyway
  • Not given commonly but won’t do any harm if farmer is persistent
48
Q

What are the main management points for reducing the incidence of milk fever in a herd?

A
  • Decrease calcium in dry period (calcium restriction)
  • decrease potassium in dry period (DCAB approach)
  • Partial vs full DCAB approach
49
Q

Explain how reducing calcium in the dry period can act as a management strategy for reducing the incidence of milk fever in a herd

A
  • Reduce in late dry period
  • Up-regulates PTH production before calving, adapt to low calcium, increased GI uptake of calcium
  • MUST increase dietary Ca at calving
  • Can be difficult to keep dietary Ca low enough, esp. due to unpredictability of grass Ca
  • Can add Ca binder to feed, but this is expensive
50
Q

Explain how reducing potassium in the dry period can act as a management strategy for reducing the incidence of milk fever in a herd

A
  • DCAB approach
  • Decrease Na and K, increase Cl and S
  • Slight acidosis increases binding of PTH and up-regulation of calcium resorption from bone
  • Increase solubility of calcium in blood and bone fluid
  • Must provide adequate Ca in dry period as there is increased metabolism
51
Q

Why does acidosis increase binding of PTH?

A

Changes shape of receptor in bone

52
Q

Compare the full and the full DCAB approach

A
  • Depends on how acidotic we want them and what can be achieved
  • Full: no milk fever, but more complications re. diet
  • Partial: some milk fever but fewer complications re. diet
53
Q

Describe the full DCAB approach in hypocalcaemia management

A
  • Add chloride and sulphur to ration (MgCl2, MgSO4)
  • Will decreased DCAB to -100mE/kg DM
  • Monitor urine pH to check acidification
  • Only consume the ration
54
Q

Why does the full DCAB approach carry a higher risk of dietary complications than the partial approach?

A
  • For full DCAB, add Cl and S, low palatability
  • Leads to lowered intake, causing risk of NED and ketosis
  • Anionic salts reduce palatability and therefore reduce DMI
55
Q

When are cows most at risk of negative energy balance and why?

A
  • Early lactation: pre-calving decrease in food intake, rapid increase in milk production, unable to keep up
  • Peak lactation: high yielding cows, difficult to consume enough energy
56
Q

What are the consequences of subclinical milk fever?

A
  • Increased risk of uterine infection
  • Increased risk of abomasal disease
  • Decreased DMI
57
Q

Discuss the diagnosis of subclinical milk fever

A
  • Difficult
  • Cannot use metabolic profile bloods
  • Control usually restored within 2-3 days of calving
  • Monitoring mainly: incidence rate of clinical cases, blood sampling of cows within 48hrs of calving, urine macromineral testing
58
Q

What is a typical aim for the number of clinical cases of milk fever?

A

<5cases/100 cows/year

59
Q

Discuss the ideal body condition score for a cow at calving

A
  • 2.5-3 at calving, avoid calving cows >3
  • Idealy no change during dry period (unless on purpose, otherwise aim for stability), and max 0.5BCS point loss after calving up to peak lactation
60
Q

What factors are monitored in order to assess a herd for metabolic disorders?

A
  • BCS
  • Metabolic profiles
  • Milk parameters
  • Ration analysis
  • Diagnosis of clinical and subclinical milk fever
61
Q

Discuss the use of metabolic profiles in the monitoring of a herd of cows for metabolic disorders

A
  • Blood sample random group of cows at specific stages (e.g. transition cows and fresh calvers)
  • Look for indicators of NEB e.g. BHB or NEFAs
  • Take approx. 8-12 samples/group (depending on size of group)
  • Target prevalence of high BHB/NEFA usually 10-20%
62
Q

How would you interpret a result of 4 of 12 samples being high for BHB and NEFA in a sample of cows?

A

Consider positive for a metabolic problem in the herd (usually consider 3 out of 12 samples a problem)

63
Q

Why is BHB assessed in metabolic profiles for a herd of cows?

A

Ketone body, indicates current energy supply/demand, esp. important in fresh calvers

64
Q

Why are NEFAs assessed in metabolic profiles for a herd of cows?

A

Are the transport form of fat, indicates mobilisation of body fat, esp. important in transition cows (indicates are already mobilising fat or are overfeeding and storing lots of fat)

65
Q

What milk parameters are assessed for the monitoring of metabolic disorders in a herd?

A

Protein and butter fat

66
Q

How are milk parameters assessed?

A

Individual milk samples, collected by the farmer (cheap)

67
Q

What would be expected to happen to the protein and butterfat in a milk sample of a a cow in NEB?

A
  • Protein down (used as energy source)

- Butterfat may increase (lots of body fat mobilised)

68
Q

Evaluate the use of milk parameters for the monitoring of herd level metabolic disorders

A
  • Protein and butter fat can be affected by many other factos e.g. milk yield (increased yield leads to decrease in both), diet (straw leads to increased butterfat due to acetate being higher)
  • Can be done as ratio, but not evidence for connection
69
Q

Discuss the use of ration analysis for the monitoring of herd level metabolic disease

A
  • Estimate feed intake and ration energy density
  • Compare to cow energy requirements
  • Use of specialist software
  • Feed intake usually as DMI
70
Q

Discuss ways of improving dry matter intake in a herd

A
  • Improve feed access (including social factors)
  • Minimise group changes (stress
  • Avoid fat cows esp. around calving
  • maximise ration palatibility (dryness, taste, chop length, variety etc.)
  • Mixed rations
  • Artifical lighting/day length
  • Avoid high ambient temperatures
71
Q

Give approximate values for the ideal DMI of a cow at peak lactation and in the transition (late dry) period

A
  • At peak lactation: >0.03kg DM/kg BWT/ day (for 700kg cow, >23kg)
  • In transition period: 0.017kg DM/kg BWT/day (for 700kg cow, >12kg/day)
72
Q

What measures can be taken to lower the incidence of metabolic disorders at a herd level?

A
  • Improve DMI
  • Assess energy density of diet
  • Additive solutions
73
Q

Discuss the assessment of energy density of the diet with regards to minimising herd level metabolic problems

A
  • Carefully formulated
  • Problems usually occur due to poor mixing/feeding technique, calculation of ration ratios, if element of ration has changed (silage varies throughout the year), wetness of feed
74
Q

Discuss the use of additive solutions with regards to minimising herd level metabolic problems, and give examples

A
  • Dietary additives can improve the situation
  • e.g. Propylene glycol, methionine linoleic acid, monensin
  • Cannot solely use concentrates and remove forage, as will move away from NEB but end up with subacute ruminal acidosis (SARA)
75
Q

What is the mechanism of action of propylene glycol as a dietary additive for the management of metabolic disorders?

A

Alternative glucose source, but expensive and only for individuals/small groups

76
Q

What is the mechanism of action of methionine as a dietary additive for the management of metabolic disorders?

A

Improves export of fat from liver

77
Q

What is the mechanism of action of Linoleic acid as a dietary additive for the management of metabolic disorders?

A

Fatty acid with less tendency to accumulate in the liver

78
Q

What is the mechanism of action of monensin as a dietary additive for the management of metabolic disorders?

A

Antibiotic, increases propionate:acetate ratio, available as a rumen bolus in UK and licensed for use in cow/heifer expected to develop ketosis

79
Q

What is DCAB?

A

Dietary cation-anion balance, i.e. the difference between the levels of major cations (Na, K) and aniona (Cl and S) in the diet, and is given as mEq/kg DM

80
Q

What DCAB can prevent hypocalcaemia and how does this work?

A

Aim for low DCAB (<0mEq/kg DM), as this induces mild metabolic acidosis and thus prevents hypocalcaemia as Ca mobilisation mechanisms become more efficient

81
Q

Describe the partial DCAB approach in the management of hypocalcaemia

A
  • Manipulate available feeds to decrease ration DCAB to around 0-100mEq/kg DM
  • +/- small amount of anionic salt
  • Choose feeds with inevitably low DCAB and use as base of diet
  • Little/no grass silage, lots of concentrate with good DCAB
  • Maize silage and straw also good
  • Can add some anionic salts to reduce DCAB furhter
82
Q

Explain how restriction of calcium can prevent hypocalcaemia

A

Conditions homeostatic mechanisms so that they are very efficient at mobiliastion i.e. lots of PTH

83
Q

Discuss the use of calcium restriction in the prevention of hypocalcaemia

A
  • Is the traditional method, during late dry period starve cow of calcium
  • Works well if can get Ca intake low enough
  • Difficult with normal transition diets due to grass, grass silage
  • Ca binding feedstuffs can be useful if feed appropriate kg per cow per day but expensive
84
Q

What are the ideal calcium levels when carrying out a calcium restriction method for hypocalcaemia management? How much calcium does a lactating cow need?

A
  • Ideally <20g/day, some effect at 40-50g/day

- Lactating cow needs >100g/day

85
Q

Discuss the use of magnesium supplementation in the prevention of hypocalcaemia

A
  • Mg required for prod. of PTH

- Not very effective by itself, unless Mg deficiency identified as a problem

86
Q

Evaluate the use of prophylactic treatment in the prevention of hypocalcaemia

A
  • Only for susceptible/targeted individuals e.g. history of milk fever, older cows etc.
  • Time consuming, often miss cases but can be useful
  • Boluses more useful for prophylaxis compared with injection
87
Q

What advice would you give to a farmer to avoid hypocalcaemia, where the silage being given a high DCAB?

A
  • Add anionic salts e.g. MgCl2, MgSO4 (but expensive and unpalatable)
  • Add calcium alone to the diet
  • Add concentrates BUT detrimental to rumen microflora so limited use
  • Swap in another silage and forages , add Brewer’s grains, concentrates and some anionic salts
88
Q

A farmer is producing his own silage. What advice could you give that would help the farmer produce low DCAB grass/silage

A

Limit fertiliser use

89
Q

What are the disadvantages of bulk milk tank analysis in the monitoring of energy balance?

A

High variation depending on how many cows are in early or late lactation, yield etc.

90
Q

Outline the use of milk fat:protein ratio in the assessment of herd level NEB

A
  • protein low due to dilution, butterfat also low so ratio unchanged
  • Protein low due to NEB, butterfat normal/high so ratio high
  • High FPR (1.4) at first recording of lactation has been associated with NEB at herd level
91
Q

Outline the full list of differential diagnoses for recumbent ewes late in pregnancy

A
  • Pregnancy toxaemia
  • Hypocalcaemia
  • Copper toxicity
  • Sodium toxicity
  • Infectious
92
Q

What are the clinical signs of pregnancy toxaemia/ketosis in sheep?

A
  • Depressed, lethargic, recumbent
  • Anorexia
  • Hypereasthesia
  • Ears twitching
  • Fine tremors
  • Reduced/absent menace
  • Low BCS
  • Pyrexic
93
Q

Describe the testing carried out for pregnancy toxaemia in ewes

A
  • Heparin blood sample

- Testing for beta-hydroxybutyrate and calcium

94
Q

Describe the practical aspects in the management required to prevent pregnancy toxaemia in ewes that can be implemented at the time of diagnosis

A
  • Find out the nutritional content of the food and adjust if needed
  • Drench sick ewes prophylactically
  • Clean bedding
  • Provide more feed
  • Separate sick ewes from rest
  • ## Ensure enough trough space (30-45cm per sheep)
95
Q

Outline the relationship between pregnancy toxaemia and BCS

A

More likely to happen in fatter ewes (lots of fat stores that can be mobilised), also more likely in thin ewes (already in negative energy balance). Ideally aim for BCS 2.5-3

96
Q

Outline the relationship between pregnancy toxaemia and BCS

A

More likely to happen in fatter ewes (lots of fat stores that can be mobilised), also more likely in thin ewes (already in negative energy balance). Ideally aim for BCS 2.5-3

97
Q

What would the following biochemistry results be indicative of in a ewe?
High BHB, normal urea, normal ALB normal Ca

A

Pregnancy toxaemia

98
Q

Give potential reasons for insufficient energy intake by ewes leading to NEB

A
  • High stocking density
  • Unpalatability of food
  • Unknown/low DMI
  • Inappropriate feeding for number of lambs each ewe is carrying
99
Q

What measures can be taken to prevent pregnancy toxaemia occurring?

A
  • Scan and feed appropriate to parity of sheep
  • identify any that are losing condition early and manage individually
  • Ensure enough food is available for all individuals, with enough space to access it
100
Q

Why might corticosteroids be used in the treatment of pregnancy toxaemia?

A

To induce abortion and therefore save the ewe rather than lose ewe and lamb

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