Endocrinology

Question 1

EMS phenotype

Answer 1

Regional adiposity or generalized
Insulin resistance (hyperinsulinaemia/abnormal glycaemic/insulinaemic responses)
Laminitis

Question 2

Development of EMS

Answer 2

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

Question 3

What does long term feeding of non-structural carbohydrates do

Answer 3

Decreases insulin sensitivity and adiponectin concentrations in comparison to forage/fat rich diets

Question 4

What breeds are genetically predisposed to insulin disregulation

Answer 4

Spanish horses- Andalusian, mustang, paso-fino
Genotype also likely to present in UK native breeds, Arabs and Caspian horses

Question 5

Problems further to ID

Answer 5

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

Question 6

Age prevalence for ems

Answer 6

5-15

Question 7

Pathophysiology of EMS

Answer 7

Adiposity - insulin resistance - laminitis

Question 8

3 stages of insulin resistance

Answer 8

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

Question 9

IR leading to laminitis

Answer 9

Change in cytokine production leads to inflammatory and pro-oxidative state including in the lamellar tissue

Question 10

Diagnostics for EMS

Answer 10

Basal glucose/insulin
Oral sugar test
CGIT

Question 11

Treatment for EMS

Answer 11

Weightloss!
Laminitis management
Farrier
Diet
Exercise
Medication
- metformin
- levo-tyroxin

Question 12

What age does PPID effect

Answer 12

18-25 (min 7)

Question 13

What is PPID

Answer 13

Benign hyperplastic neoplasia of the pars intermedia due to micro/macro adenoma formation reducing dopamine inhibition if hypophyseal melanocytes

Question 14

aMSH

Answer 14

Causes adipose deposition in different places. Reduces the cytokine response an can lead to obesity due to interference with the appetite satiety balance.

Question 15

What is B-endorphin

Answer 15

Endogenous steroid associated with dull mentation

Question 16

Clinical signs of PPID

Answer 16

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)

Question 17

Midterm/advanced cases

Answer 17

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)

Question 18

Diagnosis of PPID

Answer 18

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)

Question 19

Sampling considerations with PPID

Answer 19

Stress/excitement effects ACTH
Severe pain can affect results
Do not test within 24-48h after sedation

Question 20

How to do a baseline acth

Answer 20

Single sample
EDTA blood onto ice/refrigerated in car
Centrifuge in 4 hours

Question 21

Thyrotropin release hormone test

Answer 21

Collect baseline in EDTA
Inject 0.5mg (<250kg) or 1mg (>250kg) TRH
Collect second 10 mins later and/or 30 mins later

Question 22

Standard Treatment for PPID

Answer 22

Pergolide dopamine agonist
Recheck ACTH after 30 days (if normal or trending down continue), if increased or the same increase dose 1-2micrograms/kg

Question 23

Treatment options for PPID

Answer 23

Pergolide
Adding cyproheptadine
Cabergoline
Chatse tree berry can improve hair coat but not a monotherapy

Question 24

What happens to ACTH in the pars intermedia

Answer 24

Converts to aMSH and CLIP

Question 25

How does it occur

Answer 25

Neurodegeneration due to loss of inhibitory dopamine input from the hypothalamus leading to overproduction of ACTH/msh

Question 26

What accumulates in relation to PPID

Answer 26

a-synuclein and lipofuscin which have links to parkinson’s

Question 27

What are the physiological causes of negative energy balance

Answer 27

Decreased intakes
Increased requirements (pregnancy/lactation)

Question 28

What are the pathological causes of negative energy balance

Answer 28

Sepsis/SIRS - endotoxaemia
Azotaemia

Question 29

Diagnosis of negative energy balance

Answer 29

Triglycerides
-1.5-5mmol/L - hyperlipidemia
- >5mmol/L hyperlipaemia
Liver enzymes that may elevate
- Ggt, ALP, SDH, Bile acids
Hyperglycemia - insulin resistance

Question 30

Treatment of hyperlipaemia

Answer 30

Provide calories in any and every way
Enteral/parenteral
Pain relief

Question 31

How does EMS lead to laminitis

Answer 31

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

Question 32

Why can endocrine tests be inaccurate in initial laminitis

Answer 32

Pain can cause Stress which raises ACTH and can exacerbate laminitis