Equine endocrine diseases, laminitis and liver Flashcards
Aetiology of PPID in horses
Progressive degeneration of hypothalamic dopaminergic neurons –> get loss of control over part intermedia causing hyperplasmia and adenoma in pars intermedia
Then pars intermediate produces lots of POMC and get elevation in peptides including ACTH
Clincial signs of PPID
Pathognomic one = hypertrichosis
Coat retentino
Chronic laminitis
Why are reference values for basal ACTH different with time of year
There is natural pituitary hyperactivity in autumn
Why do we have a grey zone of ACTH concentration resutls
Up to 25% of PPID horses fall in grey zone
Up to 30% non-PPID horses in grey zone
So interpret in context of clinical signs
Allows higher sensitivity
What age animals are more likely to have false +ve for PPID
young
When not to test a horse for PPID
IF it has had severe pain for 24 hrs or more
If it has travelled in past 12hrs
Treatment of PPID
= pergolide
To replace dopaminergic control of pars intermedia
2microg/kg/day
Side effects of pergolide treatment
Transient inappetance
- If get this can stop and restart at a lower dose after 2 week washout
Reduced milk production; stop treatment for 6 weeks pre-partum
How do we monitor success of pergolide in managing PPID
CHeck ATCH concentration
Insulin and clinical assessment
- Increased insulin very important in laminitis so this is key clinical outcome; if insulin is still high, more likely to continue increasing pergolide dose than with high ACTH but good insnulin control
Why is it important to keep on top of dentistry in PPID horses
To ensure they keep eating well and issues are picked up sooner
What is equine metabolic syndrome
Collection of risk factors for hyperinsulinaemia assocaited laminitis
Consident feature = insulin dysregulation
Mixture of environment and genetics
Which horses are at high genetic risk of EMS
Miniature horses, native ponies, warmbloods
- Only need more mild environmental influences to provoke EMS
Signs of subclinical laminitis
Divergent rings; wider at heel than front of foot = marker of historic laminits
Footsore after trimming.
doesn’t like hard ground
How long do divergent rings take to appear after laminitis
3 months
Lab tests for EMS
Unfasted sugar = low sensitivity test
Dynamic test = karo syrup challenge
–> Fast then give Karo light corn syrup and take sample to test for glucose, insulin, trigylcerides an hour later
Adiponectin test = for adipokine peptide
> Low levels assocaited with EMS and metabolic obestiy
What adiponectin levels are assocaited with EMS
<7.9microg/ml
Diet for EMS horse
Starch and sugar must make up <10% of diet
IF overweight want to lose weight but can’t let dry matter intake go below 1% body weight
Haylage is a good option
Medications for EMS (increasing risk level)
Metformin: impairs glucose absorptions and reduces insulin response to glucose ingestion
Levothyroxine speeds up metabolism
Gliflozins block glucose uptake rom renal filtrate [take care since liver disease risk]
What side effects are there with levothyrozine for EMS treatment
Makes horses hyperthyroid so if stopping can get hypothyroiism
High doses can make horses fizzy; excitable, box walking
When might we use Gliflozins in EMS treatment
In an emergency with very high laminitis risk; because very good at bringing insulin down via blocking glucose uptake from renal filtrate
BUT: there are reports of peracute liver disease
Also risk of bringing triglycerides up too high
What happens at a cellular level with acute laminitis
Disturbance of lamellar attachment between hoof and foot
- In endocrinopathic laminitis: there is epithelial cell stretch
- IN sepsis relted laminitis get basement membrane detachment
What is type 1 laminitis
Can affect any horse
Related to endotoxin/sepsis Or to weight-bearing e.g with fracture repair or lymphantisi
Rapid loss of adhesions and cytoskeleton failure
How is endocrinopathic laminits different to type 1
= more mild insidious onset
Slow progressive lamellae lengthening via stretch and cellular proliferation
What can recumbent laminitics show on bloods that may make it look like myopathy
Modest CK/AST elevations
Sgins of foot pain
Reluctance to move, more recumbency, stiff fait, rocking backwards stance off of front limbs
Hot hoof walls, digital pulses, divergent rings, dropped soles, tachycardia, sweating etc
Treating laminitis
- Treat underlying condition e.g sepsis, insulin dysregulation (EMS)
- Minimise lamellar damage via anti-inflammatories and confinement
Why don’t we walk out laminitic horses
Can rip the lamellar attachments
What are some potential adverse consequences of NSAID use e.g in laminitis management
Glandular disease of stomach, colitis
Kidney injury; check creatinine/SDMA a week in
What is part of the pentafusion CRI that a horse might be given in hospital
ACP, morphine, ketamine, detomidine, lidocaine
What is the aim with boots in laminitis
To redistribute the load bearing to the caudal 1/3 of the foot
Do this as soon as foot can be picked up for a few seconds
How should a farrier foot trim a laminitic horse
Nip heels down to move weight bearing to back of foot
Trim toe to make braking easier and putting less pressure on flexor tendon –> in turn pedal bone and lamellae
How are steward clogs useful in laminitis
Allow horses to weight bear through a smaller footprint + reduces shear forces
What views of feet should we take in laminitis assessment
LAteromedial
Dorsopalmar
- All 4 feet
What is hepatic encephalopathy
When increase in ammonia delivered to brain due to liver disase/portosystemic shunt causes astrocyte swelling
Clinical signs of hepatic dysfunction in horses
LEthargy
Weight loss
Colic
Photosensitisation
Encephalopathy
Jaundice?
Odema due to low albumin
Coagulopathy?
If we see jaundice in a horse what does this generally mean
Haemolytic anaemia
Which biochemical parameters are liver specific
GGT
GLSH
[vs ALP which increases with gut issues, bone remodelling
And AST which increases with muscle issues]
If we want to see if high AST is related to liver to muscle what can we look at
Check CK; if CK high then probably due to muscle damage not liver
In what liver disease might blood tests look more severe than they actually are
Reversible liver disease due to mycotoxin exposure
Wen to NOT do a liver biopsy
- With hepatic lipidosis due to risk of rupture of liver
With recent colic; because may just be this causing raised GGT not a liver issue
How can we tell a horse probably has hepatic lipidosis and so we shouldn’t biopsy
BLood looks like strawberry smoothie and serum is opaque when spun down
How many liver biopsies to take
Want 10 portal tracts
- This means 2 (if good i.e all liver) or 3 biopsies
What are some potential complications if liver biopsy is done blind
Haemorrahge, peritonitis, colic, pneumothorac, pleuritis
What would marked eosinophilic infiltrate on liver histopath tell us is going on
multisystemic eosinophilic epitheliotrophic disease (MEED)
What liver disease would it be a good idea to give antibiotics for and what do we see on biopsy
Septic cholangiohepatitis
See neutrophilic portal infiltration
What do we see on biopsy with ragwort toxicity
Megalocytosis i.elarge liver cells with enlarged nuclei
In reality this is probably over-estimated how often this occurs; often biopsy not done
When might we see haemosiderin deposition in horse liver biopsy
Where owners have given excess dietary iron in supplements which is laid down in liver
Treating haemosiderin deposiiton in liver
Therapeutic phlebotomy every 2 weeks to create iron drain and allow redistribution from liver
What does a chronic active hepatitis biopsy look like and how do we treat
Mononuclear infiltrate in portal areas
Treat with steroids, azathioprine
What does spotty necrosis on liver biopsy suggest about cause of disease
Toxic insult e.g aflatoxin
What is a common biopsy finding where there are liver dsiase outbreaks in a field
Aflatoxin
See focal aggregates of neutrophils in parenchyma
