Endocrine + Metabolic Disorders Flashcards
Explain the pathophysiology of equine metabolic syndrome (EMS).
Horses which have breed disposition for EMS have thrify genes that allow them to survive harsh winters - have to be a breed predisposed to get EMS.
Feed abundance in autumn leads to increased adipose stores and insulin resistance as a metabolic preparation for winter, however domesticated horses dont tend to get fed less throughout the winter so the temporary effects of that insulin resistance becomes permanent and leads to the clinical disease of EMS.
Describe the link between insulin dysregulation + endocrinopathic laminitis.
Hyperinsulinaemia stimulates insulin-like growth factor-1 receptors in the hoof lamellae which leads to cellular proliferation + lamellar attachment weaknening, eventually –> lamellar failure and endocrinopathic laminitis as a result.
How do we diagnose insulin dysregulation in equids?
Excessive insulin response to non-structural carbohydrates - do an in-feed glucose challenge or oral sugar testing ;insulin >60uU/ml
Fasting baseline insulin level >10uU/ml
Baseline insulin post-feed >30uU/ml
Which breeds and age group have genetic predisposition to EMS?
6-20yo
WELSH PONIES, Dartmoor, New Forest, Shetland Ponies
Morgans
Arabians
Warmbloods
May be seen in TBs > QH > STB (very unlikely)
Describe the average clinical presentation of an EMS pony/horse.
Obese - BCS >6/9 + reduced exercise
Regional adiposity - tail base, flanks, cresty neck
So called “easy keepers”
Laminitis (usually pasture associated with no obvious initiating cause) or previous history of laminitis
Usually seasonal - late spring, early summer
Discuss the management of a clinical case of EMS.
Weight reduction - exercise them (lunging is good unless they are lame), decrease intake (put them in a negative energy balance if they are obese), remove from pasture/restrict access, confine to a small grass paddock within a larger paddock and limit grazing to 1hr up to 3x/day, use a grazing muzzle
Decrease non-structural carbs in diet - should be <10% of diet, remove grain + concentrated, remove excessive consumption of carrots/apples, no pasture access in risk seasons, restrict grazing times to late night/early morning, soak hay to remove sugars
If not obese then use feeds with moderate NSC content - soaked beet pulp, soy hulls, rice bran
Medicate with SGLT2-inhibitors (ertugliflozin 0.05mg/kg PO SID, canagliflozin) if management changes are not effective after 6 weeks or if the horse has concurrent HAL and cannot be exercised
Levothyroxine can be used to assist with weight loss + improved insulin sensitivity but is $$$$
Metformin to dec. intestinal absorption of glucose
How does ertugliflozin help manage EMS? What are the potential side effects?
It decreases glucose and insulin concentrations by reducing renal re-absorption of glucose and promotes glucosuria.
Side effects - hypertriglyceridaemia, PU/PD, increased risk of UTI
Describe the common signalment and clinical presentation of a horse with PPID.
> 15yo
HYPERTRICHOSIS
Hyperhydrosis
Supraorbital fat pads/bags under eyes
Weight loss + wasted topline
Pot belly
PU/PD
Lethargy
Inc. recovery times from illnesses
Laminitis
Less commonly blindness, seizures, infertility, collapse
Explain your diagnostic approach to PPID.
If a horse has clinical signs and a hx that makes you suspicious of PPID then measure endogenous ACTH
If its a high positive >70-120pg/ml (depending on time of year) then there is clear evidence of insulin dysregulation –> initiate management plan
If its inconclusive/a grey zone result and the horse does not have Cx supportive of PPID –> retest in the dynamic phase (Feb-April in WA)
If ACTH >120pg/ml on retest in dynamic phase then treat for PPID
If its inconclusive and the horse does have Cx supportive of PPID –> TRH stim test
TRH stim test is positive for PPID if ACTH response at the second blood sample is >110pg/ml
Describe an appropriate treatment plan for a horse with PPID.
Pergolide at lowest possible dose
Cabergoline if horse is refractory to pergolide treatment
Regular 6 month dental checkups
Regular anthelmintic treatment based on FEC results
Aggressive treatment of infections
Farriery - 5-6 week schedule, address laminitis if present
Assess laminitis risk by measuring insulin (oral sugar test or in-feed glucose test)
If ID doesnt improve with drugs then manage as EMS horse
What are the normal triglyceride concentrations for a normal pony/horse, donkey, and pregnant pony?
Normal horse/pony triglycerides = <0.82mmol/L
Normal donkey = <3.28mmol/L
Pregnant pony = <2.85mmol/L
Describe the clinical signs associated with an early-stage case of hyperlipaemia.
Depression
Lethargy
Failure to drink
Reduced GIT motility and faecal output
Often will be associated with the primary disease if present
Describe the clinical signs associated with an mid-stage case of hyperlipaemia.
Colic
Diarrhoea
Jaundice of MM
+/- subcutaneous oedema
Hepatic encephalopathy - head pressing, persistent yawning, aimless wandering, mild ataxia
Describe the clinical signs associated with an late-stage case of hyperlipaemia. How long can it take to reach this stage of the disease?
Recumbency
Convulsions
Death
Can take days to up to 3 weeks
Describe how to diagnose hyperlipaemia.
Hypertriglyceridaemia - >5.65mmol/L
Biochem - inc. GGT, GLDH + bile acids, pre-renal azotaemia, hypoglycaemia (unless concurrent ID then probably still hyperglycaemia), slightly inc. lactate (metabolic acidaemia)
