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Michaelmas 5th year > Equine endocrine diseases, laminitis and liver > Flashcards

Equine endocrine diseases, laminitis and liver Flashcards

1
Q

Aetiology of PPID in horses

A

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

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2
Q

Clincial signs of PPID

A

Pathognomic one = hypertrichosis
Coat retentino
Chronic laminitis

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3
Q

Why are reference values for basal ACTH different with time of year

A

There is natural pituitary hyperactivity in autumn

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4
Q

Why do we have a grey zone of ACTH concentration resutls

A

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

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5
Q

What age animals are more likely to have false +ve for PPID

A

young

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6
Q

When not to test a horse for PPID

A

IF it has had severe pain for 24 hrs or more
If it has travelled in past 12hrs

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7
Q

Treatment of PPID

A

= pergolide
To replace dopaminergic control of pars intermedia
2mg/kg/day

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8
Q

Side effects of pergolide treatment

A

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

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9
Q

How do we monitor success of pergolide in managing PPID

A

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

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10
Q

Why is it important to keep on top of dentistry in PPID horses

A

To ensure they keep eating well and issues are picked up sooner

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11
Q

What is equine metabolic syndrome

A

Collection of risk factors for hyperinsulinaemia assocaited laminitis

Consident feature = insulin dysregulation
Mixture of environment and genetics

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12
Q

Which horses are at high genetic risk of EMS

A

Miniature horses, native ponies, warmbloods
- Only need more mild environmental influences to provoke EMS

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13
Q

Signs of subclinical laminitis

A

Divergent rings; wider at heel than front of foot = marker of historic laminits
Footsore after trimming.
doesn’t like hard ground

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14
Q

How long do divergent rings take to appear after laminitis

A

3 months

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15
Q

Lab tests for EMS

A

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

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16
Q

What adiponectin levels are assocaited with EMS

A

<7.9microg/ml

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17
Q

Diet for EMS horse

A

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

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18
Q

Medications for EMS (increasing risk level)

A

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]

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19
Q

What side effects are there with levothyrozine for EMS treatment

A

Makes horses hyperthyroid so if stopping can get hypothyroiism

High doses can make horses fizzy; excitable, box walking

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20
Q

When might we use Gliflozins in EMS treatment

A

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

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21
Q

What happens at a cellular level with acute laminitis

A

Disturbance of lamellar attachment between hoof and foot
- In endocrinopathic laminitis: there is epithelial cell stretch
- IN sepsis relted laminitis get basement membrane detachment

22
Q

What is type 1 laminitis

A

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

23
Q

How is endocrinopathic laminits different to type 1

A

= more mild insidious onset
Slow progressive lamellae lengthening via stretch and cellular proliferation

24
Q

What can recumbent laminitics show on bloods that may make it look like myopathy

A

Modest CK/AST elevations

25
Q

Sgins of foot pain

A

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

26
Q

Treating laminitis

A
  • Treat underlying condition e.g sepsis, insulin dysregulation (EMS)
  • Minimise lamellar damage via anti-inflammatories and confinement
27
Q

Why don’t we walk out laminitic horses

A

Can rip the lamellar attachments

28
Q

What are some potential adverse consequences of NSAID use e.g in laminitis management

A

Glandular disease of stomach, colitis
Kidney injury; check creatinine/SDMA a week in

29
Q

What is part of the pentafusion CRI that a horse might be given in hospital

A

ACP, morphine, ketamine, detomidine, lidocaine

30
Q

What is the aim with boots in laminitis

A

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

31
Q

How should a farrier foot trim a laminitic horse

A

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

32
Q

How are steward clogs useful in laminitis

A

Allow horses to weight bear through a smaller footprint + reduces shear forces

33
Q

What views of feet should we take in laminitis assessment

A

LAteromedial
Dorsopalmar

  • All 4 feet
34
Q

What is hepatic encephalopathy

A

When increase in ammonia delivered to brain due to liver disase/portosystemic shunt causes astrocyte swelling

35
Q

Clinical signs of hepatic dysfunction in horses

A

LEthargy
Weight loss
Colic
Photosensitisation
Encephalopathy
Jaundice?
Odema due to low albumin
Coagulopathy?

36
Q

If we see jaundice in a horse what does this generally mean

A

Haemolytic anaemia

37
Q

Which biochemical parameters are liver specific

A

GGT
GLSH

[vs ALP which increases with gut issues, bone remodelling
And AST which increases with muscle issues]

38
Q

If we want to see if high AST is related to liver to muscle what can we look at

A

Check CK; if CK high then probably due to muscle damage not liver

39
Q

In what liver disease might blood tests look more severe than they actually are

A

Reversible liver disease due to mycotoxin exposure

40
Q

Wen to NOT do a liver biopsy

A
  • 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
41
Q

How can we tell a horse probably has hepatic lipidosis and so we shouldn’t biopsy

A

BLood looks like strawberry smoothie and serum is opaque when spun down

42
Q

How many liver biopsies to take

A

Want 10 portal tracts
- This means 2 (if good i.e all liver) or 3 biopsies

43
Q

What are some potential complications if liver biopsy is done blind

A

Haemorrahge, peritonitis, colic, pneumothorac, pleuritis

44
Q

What would marked eosinophilic infiltrate on liver histopath tell us is going on

A

multisystemic eosinophilic epitheliotrophic disease (MEED)

45
Q

What liver disease would it be a good idea to give antibiotics for and what do we see on biopsy

A

Septic cholangiohepatitis
See neutrophilic portal infiltration

46
Q

What do we see on biopsy with ragwort toxicity

A

Megalocytosis i.elarge liver cells with enlarged nuclei
In reality this is probably over-estimated how often this occurs; often biopsy not done

47
Q

When might we see haemosiderin deposition in horse liver biopsy

A

Where owners have given excess dietary iron in supplements which is laid down in liver

48
Q

Treating haemosiderin deposiiton in liver

A

Therapeutic phlebotomy every 2 weeks to create iron drain and allow redistribution from liver

49
Q

What does a chronic active hepatitis biopsy look like and how do we treat

A

Mononuclear infiltrate in portal areas
Treat with steroids, azathioprine

50
Q

What does spotty necrosis on liver biopsy suggest about cause of disease

A

Toxic insult e.g aflatoxin

51
Q

What is a common biopsy finding where there are liver dsiase outbreaks in a field

A

Aflatoxin
See focal aggregates of neutrophils in parenchyma

Michaelmas 5th year (41 decks)

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