Endocrinology Flashcards
EMS phenotype
Regional adiposity or generalized
Insulin resistance (hyperinsulinaemia/abnormal glycaemic/insulinaemic responses)
Laminitis
Development of EMS
Excess leptin from fat constantly leads to leptin resistance which stops the animal feeling full
Adiponectin production stops so insulin doesn’t direct glucose to liver/muscle and leads to insulin resistance
What does long term feeding of non-structural carbohydrates do
Decreases insulin sensitivity and adiponectin concentrations in comparison to forage/fat rich diets
What breeds are genetically predisposed to insulin disregulation
Spanish horses- Andalusian, mustang, paso-fino
Genotype also likely to present in UK native breeds, Arabs and Caspian horses
Problems further to ID
Poorer prognosis for laminitis recover
Mesenteric lipoma formation leading to strangulating SI lesions
Increased risk of hyperlipaemia
Impaired thermoregulation
Altered oestrus
Greater risk of OCD in their foals
Age prevalence for ems
5-15
Pathophysiology of EMS
Adiposity - insulin resistance - laminitis
3 stages of insulin resistance
Compensated IR - normal glucose a insulin levels increase
Uncompensated - glucose increases and insulin increased
Type 2 diabetes mellitus - end stage, persistent hyperglycemia due to inadequate insulin output
IR leading to laminitis
Change in cytokine production leads to inflammatory and pro-oxidative state including in the lamellar tissue
Diagnostics for EMS
Basal glucose/insulin
Oral sugar test
CGIT
Treatment for EMS
Weightloss!
Laminitis management
Farrier
Diet
Exercise
Medication
- metformin
- levo-tyroxin
What age does PPID effect
18-25 (min 7)
What is PPID
Benign hyperplastic neoplasia of the pars intermedia due to micro/macro adenoma formation reducing dopamine inhibition if hypophyseal melanocytes
aMSH
Causes adipose deposition in different places. Reduces the cytokine response an can lead to obesity due to interference with the appetite satiety balance.
What is B-endorphin
Endogenous steroid associated with dull mentation
Clinical signs of PPID
Muscle atrophy of postural muscles
Hair abnormalities - retained hairs as more in anagen phase. Dull coat
Dull, lack of energy, poor performance - B-endorphin
Regional adiposity - aMSH (retrobulbar space, tail head, dorsal ribs, nuchal crest)
Midterm/advanced cases
Metabolic shift - hyperinsulinaemia and laminitis.
Secondary bacterial infections - bacterial sinusitis, skin infections, foot abscess, bronchopneumonia, high parasite burden
Hyperhidrosis/anhidrosis - pars Nervosa compression decreasing ADH release
Hypertrichosis (pathognomonic)
Diagnosis of PPID
Resting ACTH (less sensitive in early stages and cut offs change through the year)
TRG is more accurate and costly (doesn’t work in autumn/early winter)
Sampling considerations with PPID
Stress/excitement effects ACTH
Severe pain can affect results
Do not test within 24-48h after sedation
How to do a baseline acth
Single sample
EDTA blood onto ice/refrigerated in car
Centrifuge in 4 hours
Thyrotropin release hormone test
Collect baseline in EDTA
Inject 0.5mg (<250kg) or 1mg (>250kg) TRH
Collect second 10 mins later and/or 30 mins later
Standard Treatment for PPID
Pergolide dopamine agonist
Recheck ACTH after 30 days (if normal or trending down continue), if increased or the same increase dose 1-2micrograms/kg
Treatment options for PPID
Pergolide
Adding cyproheptadine
Cabergoline
Chatse tree berry can improve hair coat but not a monotherapy
What happens to ACTH in the pars intermedia
Converts to aMSH and CLIP
How does it occur
Neurodegeneration due to loss of inhibitory dopamine input from the hypothalamus leading to overproduction of ACTH/msh
What accumulates in relation to PPID
a-synuclein and lipofuscin which have links to parkinson’s
What are the physiological causes of negative energy balance
Decreased intakes
Increased requirements (pregnancy/lactation)
What are the pathological causes of negative energy balance
Sepsis/SIRS - endotoxaemia
Azotaemia
Diagnosis of negative energy balance
Triglycerides
-1.5-5mmol/L - hyperlipidemia
- >5mmol/L hyperlipaemia
Liver enzymes that may elevate
- Ggt, ALP, SDH, Bile acids
Hyperglycemia - insulin resistance
Treatment of hyperlipaemia
Provide calories in any and every way
Enteral/parenteral
Pain relief
How does EMS lead to laminitis
Hyperglycemia leads to hyperinsulinaemia. Excess insulin in the blood leads to excess MMP production which increases the risk of laminitis by causes the laminae to move
Why can endocrine tests be inaccurate in initial laminitis
Pain can cause Stress which raises ACTH and can exacerbate laminitis
