Endocrinology Flashcards
Physiological causes of negative energy balance
Decreased intake
Increased requirements
Pathological causes of negative energy balance
Sepsis
Azotaemia (pre-renal)
Diagnosis of hyperlipaemia in the horse
Elevated triglycerides (1.5-5mmol/L = hyperlipidaemia, >5mmol/L = hyperlipaemia)
Blood serum discoloured
Liver enzymes may be elevated (GGT, ALP, SDH, bile acids)
Hyperglycaemia due to insulin resistance
Treatment of hyperlipaemia
Provide calories (enteral: hand feeding/any feed or parenteral: glucose infusion even if hyperglycaemic)
Treatment of primary condition (pain relief)
Enteral feeding options in hyperlipaemia if costs are limited
Nasogastric tubing soaked pelleted feed
Nasogastric tubing powdered glucose/galactose
Syringe feeding into mouth (dextrose powder/treacle/apple sauce)
What is hyperlipidaemia?
Precursor to hyperlipaemia, must be proactive
Triglycerides 1.5-5mmol/L
Mechanism of PPID
Neurodegenerative disease
1) Lack of inhibitory dopamine from hypothalamus
2) Hyperplasia and adenoma formation (benign neoplasia)
3) Overproduction of POM-c
4) Over production of ACTH/MCH
What is cushings disease referring to in the horse?
PPID/pituitary pars intermedia dysfunction
Difference between cushings in the dog and cushings in the horse
ACTH increase in the horse, but no cortisol increase
Signalment for PPID
18-25 years old
Ponies and Morgans predisposed
Pathophysiology of sedated/quiet attitude in PPID
B-endorphin has opioid activity
Pathophysiology of abnormal adipose deposition in PPID
alpha-MSH
Early signs of PPID
Muscly atrophy (loss postural muscles = pot belly appearance)
Hair abnormalities
Dull, lack of energy, poor performance
Regional adiposity
Pathophysiology of hair abnormalities in PPID
More hair in anagen phase
Where do horses retain long hair when they have PPID?
Jugular furrow
Submandibular furrow
Pastern area
What is pathognomic for PPID
Hair coat abnormalities
Metabolic changes in advanced PPID (2)
Hyperglycaemia
Hyperinsulinaemia
What disease would you be suspicious about in an older horse with an infection that is unusually difficult to treat (dental disease/skin infection/surprisingly high parasite burden/foot abscess etc.)?
PPID
Pathophysiolgy of hyperhidrosis in PPID
Catecholamine release
Long hair coat
Pathophysiology of pseudolactation in PPID
Prolactin is controlled by dopamine, there is loss of dopamine control in PPID
Some uncommon signs of PPID
PUPD (compression of pars nervosa –> decreased ADH release)
Hyperhidrosis
Pseudolactation
Suspensory ligament breakdown (collagen II)
Central blindness (adenoma compression)
Narcolepsy
Low fertility/irregular cycling
If a horse with PPID is obese, what should be measured?
Insulin levels (looking for hyperinsulinaemia which predisposes to laminitis)
Options when testing for PPID
Resting ACTH
TRH stimulation test
Benefits of resting ACTH test in PPID
One blood sample
Quick
Cheap
Well established reference ranges year round
Problems with resting ACTH test for PPID
Less sensitive in early stages
Affected by stress/excitement/severe pain/after sedation)
Important consideration when taking blood tests for PPID and choice of blood tube
Blood must be chilled, should be done on last visit of the say
EDTA
Benefit of TRH stim test in PPID
Very sensitive in early stages (use if ACTH negative with high suspicion)
Problems with TRH stim test
More expensive
Doesn’t work year round (no reference ranges established for Autumn/early winter)
Treatment for PPID
Pergolide
Action of pergolide
Dopamine agonist
Next steps if initial PPID treatment isn’t effective
ACTH test
Assess for concurrent disease
Increase pergolide dose
May consider slow release injectable form (Cabergoline)
Major predisposing factor for insulin dysregulation?
Obesity
Insulin dysregulation increases the risk of which disease?
Laminitis
EMS phenotype (3 things)
Regional adiposity or obesity
Insulin resistance
Clinical or subclinical laminitis in absence of recognised cause
Functions of adipose tissue
Leptin decreases appetite
Adiponectin sensitises tissues to insulin and downregulates inflammatory reactions
Production of cytokines (pro-inflammatory)
Problem with excess adipose tissue
Leptin released in excess –> leptin resistance –> overstimulation of appetite
Pro-inflammatory state
Problem with ‘thrifty’ gene in certain horse breeds
Predisposed to insulin dysregulation if maintained on high starch diet even if not obese (adapted to harsh diet)
Is insulin dysregulation in horses usually compensated or uncompensated?
Compensated
Problems associated with obesity and EMS
Insulin dysregulation
Poorer prognosis for laminitis recovery
Pedunculated mesenteric lipomas can cause strangulating small intestinal lesions
Hyperlipaemia
Abnormal thermoregulation
Altered oestrus cycle and reduced fertility
Foals born for obese mares have higher risk of OCD
Pro-inflammatory state affects other disorders
Three stages of insulin resistance
Compensated (normal glucose, hyperinsulinaemia)
Uncompensated (hyperglycaemia and hyperinsulinaemia)
Type II diabetes mellitus (end stage, persistent hyperglycaemia, beta cell exhaustion/inadequate insulin output)
Tests for diagnosing EMS
Basal glucose/insulin
Oral sugar test (OST)
Combined glucose-insulin test (CGIT)
Main problem with all tests for EMS
False negative common
Is EMS testing important in management of obese horses?
No, can expect insulin resistance to develop in all obese horses so should aim for weight loss regardless of EMS testing
Principles in management of EMS
Weight loss (diet and exercise)
Management of laminitis (good farrier)
Drugs can enhance weight loss in short term
Treat PPID if present (pergolide)
Drugs that can be used for weight loss in EMS (3)
Metformin
Levo-Tyroxin
Ertuglifozin? (Only preliminary studies into safety and efficacy)
Action and use of Metformin in EMS treatment
Decreases enteric glucose absorption to reduce post-prandial increase in blood glucose and insulin
Given 30-60 mins before feeding
For horses that are insulin dysregulated while management changes are put in place
(Licensed for use in humans)
Levo-tyroxin action
Increases metabolic rate to accelerate weight loss
Ertuglifloxin action
Sodium-glucose co-transporter
Targets receptors in proximal tubule of kidney to increase glucose loss in urine
Metformin licensing
Licensed for use in humans
