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ENI2 > Equine endocrinopathies 2 > Flashcards

Equine endocrinopathies 2 Flashcards

Endocrinopathic laminitis, hyperlipaemia, hyperglycaemia, obesity

1
Q

What types of conditions are risk factors for laminitis?

A
  • Pro-inflammatory conditions
  • Intestinal conditions
  • Endrocrinopathic conditions (glucocorticoid or insulin resistance associated)
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2
Q

What are the main molecular triggers for laminitis?

A

Insulin and endotoxins

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3
Q

What are the predisposing factors for lamintis?

A
  • Obestiy
  • Breed
  • Insulin dysregulation
  • PPID
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4
Q

Outline the relationship between glucocorticoids and lamiinitis

A
  • Exogenous and endogenous
  • Induce insulin resistance
  • Insulin resistance leads to increased insulin and consequent laminitis
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5
Q

Give examples of iatrogenic causes of laminitis and how these may occur

A
  • Triamcinolone (glucocorticoid) can lead to hyperglycaemia 3-4 days after 1 dose
  • Dexamethasone can increase basal insulin and induce IR over prolonged period
  • May have prolonged effects
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6
Q

Outline how PPID may predispose to laminitis

A
  • Hyperadrenocorticism, increased cortisol leading to IR

- High insulin more likely to develop laminitis

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7
Q

Outline how EMS may predispose to laminitis

A
  • Obesity, leads to insulin resistance
  • Predisposed to laminitis
  • Can be seasonal and pasture associated (seasonal obesity, lush grass spring/summer)
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8
Q

What factors may exacerbate the development of laminitis?

A
  • Progression of obesity
  • Diet rich in starches/sugars
  • Progression of PPID
  • Work on hard floors
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9
Q

Explain hyperinsulinaemia induced vasodilation as a trigger factor for laminitis

A
  • Increases perfusion to the lamellar tissue
  • Increases glucose delivery to hoof tissues (glucotoxicity)
  • Advanced glycation end products - role in human diabetic angiopathy, may play role in laminitis
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10
Q

What are the effects of insulin on blood vessels?

A
  • Balance of constriction and dilation (slight predilection for vasodilation)
  • Vasodilation via nitric oxide
  • Vasoconstriction via endothelin-1 (ET-1)
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11
Q

What are the effects of insulin resistance and corticosteroids on blood vessels?

A
  • Reduced vasodilation

- Significant vasoconstriction

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12
Q

What are the vascular consequences of hyperinsulinaemia?

A

Vasodilation leading to glucotoxicity and angiopathy

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13
Q

What molecules are raised in EMS?

A

FFas, TNFa, interleukins and leptin

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14
Q

What molecule is lowered in EMS?

A

Adiponectin

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15
Q

What is the physiological role of adiponectin?

A

Regulates glucose metabolism and fatty acid oxidation

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16
Q

What is the effect of insulin resistance on adiponectin?

A

IR leads to decreased adiponectin activity

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17
Q

What environmental factor may predispose a horse to becoming insulin resistant?

A

Moving from bare pasture to lush spring pasture (high sugar, high calories, eat more), become obese, persistently hyperinsulinaemic so become IR

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18
Q

What nutritional changes may lead to a hyperinsulinaemic crisis in a horse?

A
  • Increase in grain feeding
  • Moving to a new pasture
  • Rapid growth of pasture grass
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19
Q

Other than nutritional, what other factors may lead to a hyperinsulinaemic crisis in a horse and why?

A
  • Any increase in stress and/or inflammation
  • Stimulates HPA axis, release of cortisol
  • Change in housing, winter, disease
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20
Q

Explain the intestinal carbohydrate overload theory of laminitis

A
  • Sudden exposure to lush pasture or carb rich feeding
  • Exceed digestive capacity of small intestine (bypass)
  • Carb overload in hindgut
  • Alteration in bacterial flora = lower pH
  • Increased intestinal permeability
  • Bacterial by-products = systemic inflammation
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21
Q

What is the main bacterial by-product that leads to laminitis?

A

Matrix metalloproteinases

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22
Q

In what conditions is MMP activity increased leading to laminitis?

A
  • Endotoxaemia
  • Hypoperfusion
  • Leukocyte activation/margination in laminar blood vessels
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23
Q

Describe the effects of MMPs on the laminae

A
  • Degradation of extracellular matrix
  • Matrix cannot maintain shape or tensile strength
  • Laminae stretch and tear, causing separation at dermal/epidermal junction
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24
Q

Outline the vascular theory of laminitis

A
  • Ischaemia of laminae may be primary lesion of laminitis in carb overload model
  • Ischaemia followed by reperfusion injury, free radical formation, further tissue damage, oedema and necrosis
  • Angiopathy precedes disruption to dermal epidermal tissue
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25
Q

Outline the basic diagnostic plan for laminitis

A

1: History - carbohydrate overload?
2: Physical exam - PPID, EMS?
3: Orthopaedic exam and radiography - OBEL grading, degree of rotation
4: Endocrine testing - PPID, IR

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26
Q

When should endocrine testing for in a laminitis work up be avoided?

A

During acute painful laminitis episodes as ACTH will be high due to stress/pain

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27
Q

What management steps can be taken to address the risk factors for laminitis?

A
  • Predisposing factors: manage/treat obesity, insulin resistance, PPID, and consistent farrier care
  • Prevent exacerbation: regulate starch/sugar intake and total calories, monitor for PPID
  • Avoid triggers: avoid sudden changes in feeding practices, gradual introduction to new pastures, treat endotoxaemia and systemic inflammation
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28
Q

What management would be beneficial during an acute laminitis episode?

A
  • Treat underlying condition if poss
  • Absolute box rest until sound and beyond (1ft deep, soft sawdust bedding)
  • NSAIDs to treat inflammation and pain (flunixin, phenylbutazone)
  • Cryotherapy
  • Remedial farriery
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29
Q

Outline the use of limiting pasture grazing in the management of laminitis

A
  • Goal is to manage obesity and stop sugars exacerbating hyperinsulinaemia
  • Strategies: short turnout <1hr, grazing muzzles, strip grazing
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30
Q

Describe the key points in the use of cryptherapy for the management of laminitis

A
  • Maintain limb temperature 4degreesC for 72hr distally from carpus
  • Start ASAP, ideally before endotaoxaemia
  • Acute laminitis only
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31
Q

What is the physiological basis of cryotherapy in the treatment of laminitis?

A

Reduce metabolic rate of tissue allowing tissue to be more resistant to hypoxia which occurs with vasoconstriction, as well as decreasing cytokine production and reducing MMP activity

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32
Q

Describe the soaking of hay in the management of laminitis

A
  • Min 45min
  • Reduces amount of hydrosoluble carbohydrates in feed
  • Need to add balancer to make up for vits/mins flushed by soaking
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33
Q

In what circumstances may a laminitic horse need to stay off pasture indefinitely?

A
  • If are still hyperinsulinaemic after appropriate management
  • if hyperglycaemic and normal insulin (pancreatic exhaustion)
  • If repeated laminitis episodes
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34
Q

When would hepatic lipidosis occur in the horse and why?

A
  • RARE
  • Better synthesis of TAGs and export of VLDL vs ruminants
  • Only if FA mobilisation and synthesis exceed oxidation and VLDl excretion
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35
Q

What are the potential consequences of lipidosis and how does this impact on the clinical investigation?

A
  • Can affect hepatic function (hepatic failure, hepatic rupture)
  • CARE with biopsy
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36
Q

How is hepatic lipidosis diagnosed?

A
  • Increased serum TAG concentration
  • Biochemical evidence of hepatic dysfunction
  • US/histopathological evidence of fatty infiltration of liver (size/echogenicity)
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37
Q

What is the relationship between obesity and hepatic lipaemia in the horse?

A
  • Obese animal has more fat that can be converted to VLDLs
  • Obese animals also likely to be IR
  • IR = no inhibition of lipolysis, higher prod. of VLDLs, lower availability of LPL to clear
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38
Q

Outline the role of insulin in lipid metabolism

A
  • Inhibits lipolysis and proteolysis
  • Decreases liver glycogenolysis, gluconeogenesis and ketogenesis
  • Stimulates lipoprotein lipase (LPL)
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39
Q

Outline the role of stress in lipid metabolism

A
  • Releae glucocorticoids, catecholamines, progesterone
  • Counteract effects of insulin on lipid metabosim
  • Contribute to insulin resistance
40
Q

In what cases must hyperlipaemia always be a top differential?

A

All ponies, miniatures, or donkeys that are inappetant for even short periods of time

41
Q

Explain the physiology behind inappetance leading to hyperlipaemia

A
  • Shift into NEB
  • Use fat stores
  • Too efficient and produce too many VLDLs
  • Leads to hyperlipaemia
42
Q

What are some clinical signs for hyperlipaemia?

A
  • Generally simply quite/dull demeanour

- More variable include icterus, anorexia, weakness, ataxia, diarrhoea, colic, fever, pendent oedema

43
Q

What other conditions may commonly mask hyperlipaemia?

A
  • infections/parasitism
  • Primary colic
  • PPID
  • Laminitis
44
Q

Explain why primary colic and PPID may be risk factors for hyperlipaemia

A
  • Colic: fast patient until identify cause

- PPID: excess glucocorticoids inhibiting insulin

45
Q

In what physiological states is hyperlipaemia a greater risk?

A
  • Higher energy demand states e.g. pregnancy (late gestation) and lactation
46
Q

Explain the breed predisposition for hyperlipaemia

A
  • Minis/ponies/donkeys have relative insulin insensitivity to favour lipolysis
  • Horses more likely to develop hypertriglyceridaemia
47
Q

Explain why stress/pain is a risk factor for hyperlipaemia

A
  • Catabolic neuroendocrine response
  • ACTH, ADH, GH, catecholamines, glucocorticoids and glucagon released
  • Insulin suppression and increased lipolysis
48
Q

List some risk factors for hyperlipaemia

A
  • Obesity
  • Breed
  • Female
  • Stress/pain/disease
  • Anything that affects appetite and shifts into NEB: anorexia, intestinal parasitism, Enteritis/colic, gastrci/large colon impactions, dysphagia, peritonitis, metritis, laminitis, dental disease, hospitalisation
49
Q

Explain the physiology of VLDL production

A
  • Increased energy demand => lipolysis in adipose tissue => FFAs, non-EFAs, and glycerol
  • FFAs enter tricarboxylic acid cycle, gluconeogenesis or become TAGs
  • TAGs stored in liver or become VLDLs in blood
  • VLDLs take into tissues through LPL action, available for mobilisation where needed
50
Q

Outline the pathophysiology of equine hyperlipaemia

A
  • In hyperlipaemia, efficient synthesis of TAGs from FFAs and quick release into blood as VLDLs
  • VLDL contain greater TAG concentration in hyperlipaemia
  • LPL induces uptake of VLDLs by peripheral tissue (incl. adipose)
  • Cause of hyperlipaemia is not overproduction of VLDLs, but decreased clearance by LPL
51
Q

How does the activity of LPL change with equine hyperlipaemia?

A

Increases 2-fold with hyperlipaemia

52
Q

Explain the role of endotoxaemia in hyperlipaemia

A
  • Increases hepatic synthesis and secretions of VLDL from liver
  • Inhibits LPL activity at high endotoxin concentrations
  • Endotoxaemia often leads to hypovolaemia which will lead to azotaemia
53
Q

Explain the role of azotaemia in hyperlipaemia

A

Interferes with LPL action

54
Q

Why are obese animals more at risk of equine hyperlipaemia?

A
  • Excessive store for NEFA and FFAs
  • Release of larger VLDL concentration
  • LPL cannot keep up = hyper lipaemia
55
Q

Outline a diagnostic plan for equine hyperlipaemia

A
  • History (signalment, behaviour)

- Plasma triglyceride concentration

56
Q

At what concentration, does plasma triglyceride concentration indicate hyperlipidaemia in ponies/minis/donkeys and what is the importance of this?
(Horses?)

A
  • > 1.5-5mmol/L (130-500mg/dL)
  • Rarely results in clinical recognisable disease but high risk of hyperlipaemia
  • Can reverse and prevent hyperlipaemia at this stage
  • (horses >5mmol/L but no gross lipaemia)
57
Q

At what concentration does plasma triglyceride concentration indicate hyperlipaemia?

A

.5mmol/L (500mg/dL)

58
Q

What common abnormalities may be be found haematology/biochem in cases of equine hyperlipaemia?

A
  • Iindicators of liver disease e.g. GGT, ALP, SDH, bile acids, glucose
  • Falsely high creatinine
59
Q

Why can hyperlipaemia affect creatinine results on biochemistry?

A

Turbidity from hyperlipaemia iterferes with light/colour analysis of creatinine concentration

60
Q

What are the main goals in the treatment of equine hyperlipaemia?

A
  • treatment of underlying concurrent disease
  • Elimination of stress
  • Improvement of energy intake
  • Inhibition of fat mobilisation from adipose tissue
  • Increase TAG uptake by peripheral tissues
61
Q

Outline the approach to the treatment of concurrent disease in equine hyperlipaemia

A
  • Provide suitable analgesia to improve appetite while major disease is undergoing treatment
  • Control promary disease
  • Resolve fluid/electrolyte deficitys
  • IV nutrition (rare, expensive)
62
Q

Outline the approach to the removal of stressors in the management of equine hyperlipaemia

A
  • Remove any stress possible

- prevent herd stress factors

63
Q

What are the approaches to improving energy intake in equine hyperlipaemia?

A
  • Carb rich diet, hand grazing, sweet feeds, leafy hay, anything but avoid fat rich ideally
  • If anorexia, 4 options: dextrose, enteral nutrition, partial parenteral nutrition, insulin therapy
  • Sooner start with parenteral nutritional = better outcome, proactive
64
Q

Outline the dextrose/glucose approach to the anorexic pony with hyperlipaemia

A
  • 5% dextrose/glucose at maintenance rate
  • Unlikely to provide daily caloric req
  • suitable in first instance but not long term
  • consider risk of hyperglycaemia if IR
65
Q

Outline the enteral nutrition approach to the anorexic pony with hyperlipaemia

A
  • Nasogastric tube
  • Ready brek, complan, crush and dissolved stuf cubes via nasogastric tube
  • Any high carb, high energy food (ideally low fat)
66
Q

Outline the partial parenteral nutrition approach to the anorexic pony with hyperlipaemia

A
  • If enternal not possible e.g post-op colic surgery
  • 5% dextrose + 8.5% amino acid solution
  • Monitor glycaemia closely
67
Q

Outline the insulin therapy approach to the anorexic pony with hyperlipaemia

A
  • Hyperglycaemia only!
  • Insulin zinc suspension 0.15IU/kg SC BID
  • Increase dose by 0.05IU/kg if hyperglycaemia does not improve
  • Dubious efficacy with IR
68
Q

What has been suggested that may be used to inhibit fat mobilisation in equine hyperlipaemia?

A
  • Nicotinic acid

- Efficacy unproven in horses

69
Q

Outline increasing the TAG uptake in treatment of equine hyperlipaemia

A
  • Heparin, 40-25 IU/kg BID
  • Stimulates LPL to remove TAGs from blood
  • LPL already at ma rate in affected ponies so benefits questionable, need to monitor haemostasis regularly
70
Q

What is the prognosis for equine hyperlipaemia?

A

Poor, estimated mortality 60-100% of affected ponies

- If survives, TAGs normal within 3-10 days

71
Q

How can equine hyperlipaemia be prevented?

A
  • Avoid breeding, transporting grossly obese ponies
  • Controlled exercise and feed intake
  • Avoid drastic weight reduction
72
Q

Describe a treatment plan for partial aprenteral nutrition

A
  • Provide 50% of digestible energy requirement for maintenance as PPN
  • Provide 50% of crude protein requirement = amino acids to be provided
73
Q

Calculate components of a parenteral nutrition solution

A
  • Digestible energy requirement = 1.4 + (0.03 x bwt kgs) =Mcal/day
  • Add 20% for late pregnancy, and 70% for lactation
  • To calculate crude protein provided/day, do Digestible energy x 40 (Mcal) = amino acids
  • Subtract amino acid calories from total energy req (4kcal/g of protein) = energy to be provided from 50% dextrose solution (500g/L = 1700kcal/L)
74
Q

Outline a monitoring plan for patients receiving treatment of equine hyperlipaemia

A
  • Check blood glucose q2-4 hours for first 12 hrs of new protocol
  • Urine dipstick to check for glucose
  • Monitor plasma TAG concentrations
  • Consider blood gas analysis or measurement of plasma bicarbonate concentrations to check metabolic acidosis
75
Q

When is enteral feeding recommended over other methods in the treatment of equine hyperlipaemia, and what are the 3 approaches?

A
  • Where finances are limited
  • 1: complete pelleted food, calculate cals required, begin with 25% then increase to 50% over 3 days, soak in warm water and pump in via nasogastric tubes 1-4 times daily
  • 2: dextrose and galactose powder mixed with water and in via nasogastric tube, use insulin at the same time to prevent hyperglycaemia
  • 3: mouth feeding via syringe, can use dextrose powder in water or treacle by heating in pan with water
76
Q

What are potential risks of enteral feeding for the treatment of equine hyperlipaemia?

A
  • Reflux
  • Smaller stomach size if have been anorexic for a few days can limit amount that should be administered
  • Hyperglycaemia
  • Owner compliance/competence
77
Q

Why might haemoconcentration occur in a diabetic horse?

A

Glucosuria leads to free water loss

78
Q

Outline the medical and husbandry management of a diabetic horse

A
  • Fluids
  • Feed soaked hay and low/no concentrates
  • Continue exercise and feed intake
  • Ensure partial parenteral nutrition
  • Administer insulin as CRI or subcut injections
79
Q

Why may hyperlipaemia develop in a diabetic horse?

A
  • Low insulin output if type I

- Insulin not inhibiting hormone sensitive lipase

80
Q

When assessing a case of laminitis, how should the lameness be assessed?

A
  • Use fingers rather than hoof testers
  • Flexion tests are absolutely contraindicated
  • This is because feet will be too painful and may cause further damage
81
Q

Describe the commonly features identified in the front and hind limbs of a laminitic pony

A
  • Front: pounding digital pulses, will not lift limb, hoof wall warm, pain at pressure over coronary band
  • Hind: warm, but no digital pulses palpable
82
Q

Other than management for the condition itself, what other treatment should be provided for a horse with PPID?

A
  • NSAID, e.g. phenylbutazone to control hoof wall inflammation
  • Remedial farriery
83
Q

Outline the welfare issues associated with obesity

A
  • Increases the risk of other diseases (laminitis, derm conditions, chronic musculoskeletal conditions)
  • Inflammatory disease
  • Fat mares pass on risk of greater adiposity
84
Q

Explain how fat mares increase the risk of adioposity in their offspring

A
  • Epigenetics
  • Not born fat, but higher fat cell to muscle cell ratio
  • End up overfeeding and fat cells become a risk
85
Q

Give examples of factors that increase the risk of obesity in horses

A
  • Being on a yard with other fat horses as becomes normalised
  • The microbiome
  • Turning out on grass in the summer (overfed but undernourished, may take on 2x required calories but fewer vitamins and minerals)
86
Q

List the factors that are addressed in the management of an obese horse

A
  • Control calories
  • Maintain feed bulk
  • Provide optimal nutrition
  • Lifestyle change
87
Q

Why is calorie control required in the management of an obese horse?

A
  • Is the only way to reduce fat
  • Reduces IR
  • Reduces chronic inflammation
  • Improves health and welfare of horses
88
Q

What amount of faeces should be produced by a normal horse?

A

1-3% BW

89
Q

How can grass be restricted in horses and why is this important?

A
  • Having sparse pasture, or restricting time outside

- Most obese horses fed very little concentrate by owner, so most calories are coming from grass, esp. in summer

90
Q

Why is it important to maintain feed bulk when managing and obese horse?

A

If reduce fibre, risk stereotypies, gastric ulcers and colic, as well as increased cortisol which can lead to IR

91
Q

How can feed bulk be maintained in horses?

A
  • Soak hay to remove sugar but maintain bulk and fibre

- Replace grass with low quality forage

92
Q

What is the importance of providing optimal nutrition in the management of obese horses?

A
  • Likely to be deficient in key minerals e.g. Cu, Zn, Na, P, Ca
  • Hay deficiency in quality protein, vitamins and minerals, esp. anti-oxidants
  • Soaking hay remoes nutrients and minerals
93
Q

How can optimal nutrition be provided when managing an obese horse?

A
  • Balance vitamins and minerals using feed balancers (100g/100kg BWT)
  • Give when grazing, winter and restricted grazing, soaking hay, hay, calorie control diet
  • Barley or oat straw
  • Carrots can also be fed
94
Q

Why is wheat straw an inappropriate feed stuff for horses?

A

High levels of lignin which increases risk of impaction

95
Q

Describe the general lifestyle changes that need to be implemented in the management of an obese horse

A
  • change diet in conjuntion with exercise to increase metabolic rate
  • Protect against insulin resistance
  • Encourage winter weight loss in leisure horses
  • Pastured horses stay as fit as exercised horses (can turn out with muzzle to prevent overfeeding)
  • No rugs in winter, daily turnout, clip underneath and leave hair on top
96
Q

Suggest an exercise regime for the management of an obese horse

A
  • brisk exercise 30mins every day, 7 days a week (HR 80bpm for 30 mins), - this is protective against IR even before fat loss

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