Equine Metabolic Diseases

Question 1

Rhyme for metabolic syndrome?

Answer 1

Jack Spratt ate lots of fat;
His wife ate lots of sweeties.
He’s had a coronary
And she’s got diabetes.

Question 2

What is Equine Metabolic Syndrome?

Answer 2

Obesity or regional adiposity.
Insulin dysregulation/resistance (IR).
Subclinical or clinical laminitis.

Question 3

Compensated vs uncompensated insulin resistance.

Answer 3

Compensated:
- hyperinsulinaemia.
- euglycaemia.
- common.
- may have this at rest, or only as a response to feeding.
– EMS/PPID.
Uncompensated:
- hyperinsulinaemia.
- hyperglycaemia.
- glucosuria.
– type 2 DM (may be secondary to PPID).

Question 4

Equine Metabolic Disease and laminitis.

Answer 4

Clinical or subclinical.
Histopathologically, and clinically, differs from laminitis secondary to toxin exposure / weight bearing.
Recent research shows hyperinsulinaemia is direct cause of laminitis.

Question 5

Role of genetics in Equine Metabolic Disease.

Answer 5

Genetic predisposition for IR in hardy breeds.
IR = adaptation for survival.
Insulin is an anabolic hormone.
IR facilitates breakdown of glucose and fat stores and stimulates hepatic gluconeogenesis.
- keeps a glucose supply for vital (non insulin dependent) tissues
– CNS etc.
- ability to mobilise energy stores and prioritise vital tissues
= survival benefit if poor diet.

Question 6

EMS, IR and obesity.

Answer 6

Obesity strongly associated with IR.
Naturally would put on weight in summer and so develop IR just in time to help survival over winter.
Losing weight in winter, restoring IS in time for spring.
Due to general management, no longer subject to seasonal weight loss.
Lack of exercise - exercise promotes insulin sensitivity.
Chronic progressive obesity and chronic laminitis ensue.

Question 7

EMS clinical signs.

Answer 7

Obesity - BCS 7-9/9.
+/or Regional adiposity.
- cresty neck.
- tail head.
preputial swelling / mammary gland.
Subclinical or clinical laminitis.
Possible related disease
- hyperlipidaemia, lipoma.
Hungry.

Question 8

EMS Ddx.

Answer 8

Insulin dysregulation:
- EMS.
- PPID.
- BOTH!
Can be hard to be sure.
Hx and signalment?
Test for both.
Rare, but can be lean and IR.

Question 9

EMS diagnostic testing.

Answer 9

Resting insulin and glucose.
- used to be the first test to take.
- but many false negatives.
Oral glucose tolerance test most likely.
IV glucose tolerance test.

Question 10

Oral glucose tolerance test.

Answer 10

Starve overnight.
- or can have a bit of low quality hay.
Take resting glucose and insulin.
- can skip.
Either feed 1g/kg dextrose powder in breakfast,
Or syringe Karolyte syrup.
Continue starving.
Insulin and glucose test at 2-3hrs.
With insulin dysregulation usually then have hyperinsulinaemia and normoglycaemia.

Question 11

EMS management - diet.

Answer 11

Diet.
- low carb.
– no concentrate.
– if thin, oil.
– can have Happy Hoof or similar.
– multivitamin and mineral supplement.
– no grass, grass muzzle.
– time restriction does not work.

Question 12

EMS management - Exercise and weight control/loss.

Answer 12

Major effect on insulin sensitivity.
What if laminitic?
Weight loss:
- feed 1/3 less than were.
- not less than 1kg forage per 100kg.
- soak hay >1h – reduces calories.
- haynet with small holes.

Question 13

EMS management - Metformin.
- other pharmaceuticals

Answer 13

Multiple ways of increasing insulin sensitivity in people.
In horses, almost no bioavailability.
Aids weight loss and reduces glucose spikes by blocking SI carbohydrate absorption.
So can help return to insulin sensitivity but only by aiding weight loss.
Not used as much now.

• Levothyroxine can increase metabolic rate and enhance weight loss.
  – expensive and more difficult to get hold of in the UK.

Question 14

EMS management - SGLT2 inhibitors.

Answer 14

E.g. ertugiflozin used to help lower blood glucose levels in human, and found to lower insulin levels in horses, and being used more in tx of laminitis and EMS on cascade.
Some risks of hyperlipidaemia.
Can have dramatic results.
There are other drug options used in people with type 2 diabetes and metabolic syndrome which may habe potential in the future.

Question 15

Hyperlipaemia vs hyperlipidaemia.

Answer 15

Hyperlipaemia:
- serum triglyceride concentration excess of 500mg/dl.
- leads to fatty infiltration of liver.
- clinical signs of liver disease.
- poor px.
Hyperlipidaemia:
- increase serum triglyceride (but <500mg/dl).
- without grossly lactescent blood.
- without fatty infiltration of the liver.
- good px if reversed quickly.

Question 16

Hyperlipaemia pathogenesis?

Answer 16

TCA cycle.
- in liver, fatty acid + amino acid
=> glucose.
Glucose => glycogen stores.

Intake decreased and/or energy demands increase lead to depleted glycogen stores, so energy provided by fatty acid oxidation.
Fatty acid mobilisation triggered by:
- negative energy balance.
- stress – catecholamine and glucocorticoid release.

Risk factors:
- obesity, ponies, in foal, donkeys (hardy).
– due to excess stores of fatty acid, increase risk of IR (progesterone), EMS.

Normally, liver will use up some fat but puts any excess back into the blood supply, and fat taken up back into adipose tissue by endothelial lipoprotein lipase.
But if not enough time for enzyme to do this, too much fat in blood (hyperlipaemia hepatic lipidosis - disease of acute starvation).

Normally, insulin impedes development of hyperlipaemia by inhibiting lipolysis of adipose tissue, inhibiting gluconeogenesis in liver, activating uptake of VLDL to adipose tissue.
IR = at risk of hyperlipaemia.
- EMS.
- glucocorticoids, catecholamines, progesterone.
Get hepatic lipidosis, liver failure (worsens condition), lactescent blood, fat embolism, kidney failure, pancreatitis.

Question 17

Dx of hyperlipaemia.

Answer 17

Try to dx when hyperlipidaemia!
Identify ‘at risks’.
Prevent if possible.

Signs of depression, anorexia, ataxia, icterus.
Test blood triglyceride level.
In hyperlipaemia, opalescent blood.
Raised serum activity of liver enzymes.
Raised bile acids.

Question 18

Tx of hyperlipaemia.

Answer 18

Improve energy intake and balance.
Tx of hepatic dz.
Tx of underlying dz.
Elimination of stress, tx of concurrent dz.
Inhibition of fat mobilisation from adipose tissue.
Increased triglyceride uptake by peripheral tissues.
Wean foal, only if horse not going to get stressed about foal going.
Tempt to eat.
Enteral nutrition (pony nut soup by stomach tube).
Glucose infusion (5% at 2ml/kg/hr).
Partial parenteral nutrition.
- monitor BG hourly at first.
- insulin – sc or infusion may be required.

Question 19

1. Px of hyperlipaemia.
2. Prevention of hyperlipaemia?

Answer 19

1. 60-100% mortality.
2. Client education.
   Identify at-risks.
   Glucose infusion and insulin if required, to AVOID hyperlipaemia.

Question 20

What are factors that control calcium homeostasis?

Answer 20

Parathyroid hormone.
Vitamin D.
Calcitonin.
Parathyroid hormone related protein.

Question 20

Role of parathyroid hormone in calcium homeostasis.

Answer 20

Responds to changes in extracellular calcium concentration:
- stimulation osteoclastic bone resorption.
- stimulation calcium reabsorption in renal tubules.
- inhibition phosphate reabsorption in renal tubules.
- increases intestinal calcium and phosphate absorption (via calcitriol).
- an overall increase in calcium.

Question 21

Vitamin D role in calcium homeostasis.

Answer 21

Active metabolite.
- stimulates intestinal calcium and phosphate absorption.
- stimulates renal calcium and phosphate absorption.

Question 22

Calcitonin role in calcium homeostasis.

Answer 22

Inhibits osteoclast function during hypercalcaemia.
- importance unknown.

Question 23

Clinical signs of hypocalcaemia?
- explain.

Answer 23

Increased neuromuscular excitability.
- calcium = Na channel antagonist, so when calcium conc. low, Na channels easily activated.
– nerve and muscle fibre excitability, muscle fasciculations, tremor, tetany.
– tachycardia, but bradycardia if v. severe as reduced cardiac muscle contractility.

Question 24

Conditions associated with hypocalcaemia - synchronous diaphragmatic flutter.

Answer 24

Colloquial name = “Thumps”.
Diaphragmatic contractions synchronous with heartbeat.
After prolonged exercise.
In systemic disease.

Question 25

Conditions associated with hypocalcaemia - hypocalcaemic tetany.

Answer 25

In lactation - from 2w before foaling to weaning.
Transit tetany.
Anxiety, ataxia, tremors, seizure, dyspnoea.

Question 26

1. Conditions associated with hypocalcaemia - seizures.
2. Conditions associated with hypocalcaemia - others?

Answer 26

1. Rare, usually hypocalcaemia + sepsis.
   Poor Px.
2. Ileus.
   Retained placenta.

Question 27

Tx of hypocalcaemia?

Answer 27

Rapid administration = CV complications.
- max 2mg/kg/hr (50ml 23% calcium gluconate solution to 500kg horse in 1hr).
- calcium deficit