This is an extract of our Endocrine Specific Diseases Large Animal document, which we sell as part of our Endocrinology and Integument 2 Notes collection written by the top tier of University Of Nottingham students.
The following is a more accessble plain text extract of the PDF sample above, taken from our Endocrinology and Integument 2 Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:
Endocrine specific diseases - large animal EQUINE METABOLIC SYNDROME (EMS) EMS describes a characteristic collection of clinical signs and clinicopathological changes in equids. Affected animals typically have increased adiposity (obesity), insulin dysregulation and a predisposition to laminitis. Clinical signs??
High risk breed or 'easy keeper'. Increased adiposity
- Cresty neck
- Supra-orbital fat
- Tail fat pads. Founder lines on hooves.
- Narrower space between growth lines at top of hoof compared to the heel.
- Caused by slower growth at dorsal hoof than at heel. Seasonal pasture-associated laminitis.
There is a breed disposition - breeds described as 'easy keepers' or 'good doers' are more likely to develop EMS. Breeds most commonly affected include ponies of all breeds, Miniature horses, Morgans, Paso Finos, Arabians and Norwegian Fjords. Horses with EMS are more likely to develop
- Laminitis - pasture associated and acute laminitis.
- Pedunculated lipomas - leading to strangulating lipomas and colic.
- Hyperglycaemia. EMS is thought to begin with insulin dysregulation.
- An increased insulin response to sugars causes hyperinsulinaemia, obesity and regional adiposity and insulin resistance. Horses with PPID are also likely to have EMS, as cortisol causes insulin resistance. EMS is also a risk factor for horses developing PPID - obesity and insulin resistance are associated with low grade inflammation and pro-oxidative sate. This increases oxidative degeneration of dopaminergic neurons. PPID may therefore develop at an earlier age in obese, insulin resistant horses or horses with EMS.
DiagnosisThe oral sugar test is a field test that can be used to diagnosis horses at risk of EMS.
- The horse is fasted overnight.
- Karo syrup containing 1g/ml of digestible sugar is fed to the horse at a dose of 0.15ml/kg (75ml for 500kg).
- It is administered orally with a dose syringe.
- The blood glucose and insulin concentrations are then measured 60 minutes and 90 minutes later, or from one sample taken 75 minutes later.
- A positive result is indicated if insulin is >60uU/ml or if glucose is
?The in-feed oral glucose challenge test can also be used
- The horse is fasted overnight
- The horse is given a non-glycaemic feed (such as chaff) containing 1g/kg bodyweight dextrose powder in the morning.
- Blood is collected 2 hours after feed is consumed.
- A positive result is indicated if insulin >85uU/mL. Resting insulin levels can also be measures.
- Normal insulin levels are <20uU/mL.
- Must be done on a fasted sample.
Weight reduction in obese horses In lean or normal body fat horses, a diet that provides calories without exacerbating hyperinsulinaemia is required.
- Free-choice hay.
- Add vegetable oil for calories at 240ml twice daily. Limit pasture grazing
- A grass paddock that is 1/3 to 1/2 of an acre is suitable.
- Give a companion to reduce stress. A hay ration balancer diet is useful for weight reduction.
% body weight
Body weight (lb)
Amount hay fed (lb)
1.5 1.5 1
1200 (current) 1000 (ideal) 1000 (ideal)
18lb 15lb 10lb?
Approximate amount (1 flak = 3lb). 6 flakes 5 flakes 3 flakes
Exercise plan that includes trotting or cantering for 30 minutes a day. Medical treatment includes
- Levothyroxine sodium o Induces mild hyperthyroidism. o Indicated for short term (3-6 months) treatment whilst response to diet and exercise plan develops. Should be reserved for refractory cases to accelerate weight loss. o Dose is 0.1mg/kg, can be increased to 0.15mg/kg in extreme cases.
o COST PROHIBITIVE IN THE UK. Metformin hydrochloride o Inhibits gluconeogenesis and lipogenesis, increases fatty acid oxidation and lipolysis and increases insulin sensitivity. o Indicated for use in refractory hyperinsulinaemic horses. o Administer 30-60 minutes prior to a meal or to turnout. o Dose of 30mg/kg given orally with a maximum of 3 doses a day.
Good At higher risk of laminitis and PPID.
EQUINE ENDOCRINOPATHIC LAMINITIS Endocrinopathic laminits is characterised by mild, sometimes sub-clinical episodes leading to damage over time. Laminitis is inflammation of the epidermal laminae that attach the distal phalanx to the hoof wall. Clinical signs????
'Easy keeper' horses possibly already diagnosed with EMS. Obese horses. Horses with PPID. Founder lines. Lameness particularly of forelimbs. Laminitic stance 'standing on heels'. Digital pulse Heat in the hoof.
Pathogenesis?Hyperinsulinaemia, PPID and EMS predispose animals to developing laminitis. Obesity is also a risk factor. Obesity results in production of adipokines which can promote insulin resistance, leading to hyperinsulinaemia. Insulin is a slow vasodilator.
???When an animal is insulin sensitive, insulin interacts with endothelial cells via the phosphatidylinositol-3 kinase pathway (PI3K pathway). This results in vasodilation and nitric oxide production. When an animal is insulin resistant, insulin interacts with endothelial cells via the mitogen-activated protein kinase pathway (MAPK pathway). This results in vasoconstriction and endothelin-1 production. Vasoconstriction can cause laminitis. Hyperinsulinaemia is exacerbated during a hyperinsulinaemic crisis, for example if the animal is turned out onto new pasture, there is an increase in grain feeding, there is rapid growth of pasture grass or in response to increase in stress such as a change in housing or disease. The theoretical theory of events causing laminitis are as follows
- Horse is suddenly turned out onto pasture rich in starch and sugars.
- The starch and sugars exceed the digestive capacity of the small intestine.
- This causes carbohydrate overload in the hindgut.
- This results in alteration of bacterial flora due to a lower pH.
- It also results in increased intestinal permeability.
- Bacterial by-products are absorbed and cause systemic inflammation, including laminitis. Bacterial by-products, hypoperfusion and endotoxaemia all stimulate metalloproteinases (MMPs) production:
- Increased expression of MMPs causes degradation of the extracellular matrix.
- The laminae cannot maintain their shape or tensile strength.
- Laminae stretch and tear, causing separation at the dermal/epidermal junction.
By clinical signs, history and characteristic of horse. Radiography may reveal rotated pedal bone.
Endocrinopathic laminitic episdoes should be treated by recognition, prevention and biomechanics.
- Management of obesity and insulin resistance
- Treatment of PPID
- Good farriery.
- Avoid sudden changes in feeding practices
- Gradual introduction to new pasture.
- Treat endotoxaemia and systemic inflammation.
- Recommend non-structural carbohydrate content of <10% for hay. NSC content can be reduced by soaking hay for 60 minutes in cold water.
- Vitamin and mineral supplementation. Systemic inflammation can be treated with
- Polymixin B
PrognosisGood with management.
Buy the full version of these notes or essay plans and more in our Endocrinology and Integument 2 Notes.