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Equine Final Year > EMS > Flashcards

EMS Flashcards

1
Q

Define Equine Metabolic Syndrome?

A

Collection of risk factors associated with an increased risk of laminitis

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2
Q

Name EMS risk factors associated with an increased risk of laminitis?

A
  1. Obesity (any obese horse has greatly increased risk of laminitis. Similar pathology to cardiac disease in obese humans but the effects on the vascular system in the horse are seen in the hoof)
  2. Insulin resistance (IR) (obesity leading to IR)
  3. Predisposition toward laminitis:
  • Additional components
  • Dyslipidaemia (hypertriglyceridaemia)
  • Hypertension
  • Hyperleptinemia
  • Altered reproductive cycling
  • Increased systemic markers of inflammation
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3
Q

Which ages is EMS prevelent in?

A

5-15 years

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4
Q

Which breeds are predisposed to EMS?

A
  • Any breed affected but some predisposed
  • Ponies, minis but also Arabians, Warmbloods, native breeds (good doers genetically predisposed as they are genetically predisposed to store/build up fat)
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5
Q

What happens to the grass in spring-summer?

A

During periods of high sunshine, when sugars are produced in excess of the energy requirement of the pasture for growth and development, they are converted into storage, or reserve, carbohydrates, such as fructans and starches. Means very high in calories and more likely to become obese. A lot of sugars can mean horse remains hyperglycemia for a long time which can lead onto laminitis.

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6
Q

Where is fat seen in obesity?

A

Neck: cresty and large

Fat pads infront and behind shoulders

Cant see ribs

Supraorbital fossa full of fat

Large fat belly

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7
Q

How is obesity defined in the horse?

A
  • BCS: ≥3/5 (or >7/9)

“crest enlarged and thickened, so fat is deposited heavily in middle of neck rather than toward poll and withers… mounded appearance..crest fills cupped hand.. loses side-to side flexibility”

  • Crest has the most correlation with EMS
  • Accurate BCS may be hard in some cases with regional adiposity

Neck

Tail head

Shoulder

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8
Q

How can a neck crest be assessed?

A

Neck assessment

  • Subjective assessment
  • Mid-neck measurement - ponies
  • Circumference : heightwithers >0.71 predicts laminitis
  • Neck-to-height ratio
  • Cresty neck scoring system
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9
Q

When can EMS occur in lean horses?

A

Occasionally lean horses have EMS

Caused by an enzyme:

  • 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1)
  • Enzyme that increases local production of cortisol in adipose tissue
  • High cortisol concentration promotes insulin resistance

Alternatively pancreatic disease can result in reduced insulin production and T2DM (type 2 Diabetes mellitus)

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10
Q

Describe the pathophysiology of EMS?

A
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11
Q

What are the functions of adipose tissue?

A
  1. Main function of fat tissue is Energy storage
  2. But also has an endocrine function: Hormone production
  • Adipokines (leptin, resistin, adiponectin and apelin) Main ones we can measure clinically in bold.
  • Adipocytokines (TNF, IL-1, IL-6)
  • Increased adipose tissue= Chronic low grade inflammation
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12
Q

It is generally assumed that obesity predisposes the animal to insulin resistance. What are the 3 theories to explain this association?

A
  • Lipotoxicity theory
  • Proinflammatory theory
  • Adipokine theory
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13
Q

What is the lipotoxicity theory of obesity and insulin resistance?

A

There is a limit to how much fat can be stored in the subcutaneous area. When this is too full, fat then goes to be stored in the visceral fat

  • One the viscera has reached its limit, the fat then ends up in the portal system where it goes to the liver to be laid down
  • Causes some degree of liver dysfunction
  • Ends up in any other tissue (e.g. skeletal muscle) and causes dysfunction and disrupted signal transduction of insulin
  • Leads to lipotoxicity and IR
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14
Q

What is the proinflammatory theory of obesity and insulin resistance?

A
  • Adipose tissues reach their capacity for fat storage, which stresses them
  • Stressed adipocytes release inflammatory cytokines called adipokines
  • These alter intracellular signal transduction pathways leading to insulin resistance
  • IR
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15
Q

What is the adipokine theory of obesity and insulin resistance?

A
  • Adipocytes produce cytokines that can be classified as hormones called adipokines
  • Obesity alters the balance of adipokines produced by the adipocytes
  • Adiponectin enhances the action of insulin
  • Lower adiponectin levels contribute to IR
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16
Q

What are the consequences of insulin resistance on glucose?

A
  • Impaired glucose uptake into cells
  • Increase glucose synthesis by the liver via gluconeogenesis
  • Blood glucose levels increase
  • Hepatic insulin resistance when insulin fails to suppress gluconeogenesis
17
Q

What are the consequences of insulin resistance on lipids?

A
  • Increased lipolysis at adipose tissues. Insulin usually suppressed it, but this is lost
  • Insulin usually dampens action of HSL, but with IR, this is lost. So HSL activity is higher
18
Q

What are the consequences of insulin resistance on protein?

A
  • Amino acids used for gluconeogenesis
  • Insulin normally enhances uptake of amino acids by tissues but IR inhibits this process.
  • Amino acids used to produce new glucose
19
Q

IR caused by?

A

Down-regulation of insulin signaling by adipokines

Accumulation of intracellular lipids (lipotoxicity)

  • Skeletal muscle cells
  • Liver
  • Pancreas
20
Q

Name the 3 stages of Insulin resistance?

A

Compensated IR: Normal glucose concentrations maintained by increased insulin output (hyperinsulinaemia)

Uncompensated IR: Glucose concentrations increasing and increased insulin concentration. Insulin does not work so glucose does not go into the cell remains hyperglycaemic.

Type 2 diabetes mellitus - end stage: Persistent hyperglycaemia because of inadequate insulin output (pancreatic β-cell exhaustion) insulin stops being produced

21
Q

What is the pathophysiology of Laminitis?

A

Complex and only partially understood:

  1. Hyperinsulinaemia
  2. Endothelial cell dysfunction
  3. Inhibition of NO release by endothelial cells
  4. Endothelin-1 synthesis and sympathetic nervous activation
  5. Digital vasoconstriction
  6. Impaired glucose uptake from epidermal laminar cells
  7. Altered epidermal cell function or mitosis
  8. Matrix metalloproteinase activation (if overly active they break down lamella tissue)
  9. Pro-inflammatory/pro-oxidative state also in lamellar tissue
22
Q

Compare insulin resistance in horses to other species?

A
  • Horses remain hyperinsulinaemic for years without developing diabetes mellitus/glucosuria
  • Detect hyperinsulinaemia with normal or high-normal glucose concentrations
  • Do not develop amylin within the pancreas and progress to diabetes mellitus (compared with cats and humans)
  • Diabetes mellitus is rarely seen and when it does occur, it is often associated with PPID (older age)
23
Q

What are other complications of equine metabolic syndrome?

A
  • Infertility (issue with production of inflam cytokines which effect ability to cycle)
  • Abnormal cycle
  • Poor conception
  • Pedunculated lipomas (strangulate intestines)
  • Hyperlipaemia (some breeds when they are obese when they go in negative energy balance hyperlipaemia can happen so be careful when starving obese animals)
  • Hyperglycaemia with parenteral nutrition
24
Q

How is diagnosis of EMS made?

A
  1. confirm insulin resistance status combined with clinical signs
  2. Rule out PPID
25
Q

Resting insulin and glucose measurement is done how?

A

Resting insulin and glucose measurement (if it comes back negative it is not definitive that it doesn’t have IR)

  • Simple and cheap
  • High resting insulin strongly suggestive of IR
  • Low insulin + high glucose -> T2 diabetes
  • Little sensitivity and specificity
  • Affected by several factors
  • Stress (transport, handling, pain etc)
  • Fed/fasted
  • Season (if at pasture)
26
Q

What is the oral glucose challenge test?

A
  1. Fast overnight (12h)
  2. Administer non-glycaemic feed (chaff) with

1g/kg glucose powder orally

  1. Measure Insulin at 2h (if IR the pancreas with increase too much insulin >85units per ml)

Insulin ≥ 85 IU/mL indicative of IR

Test convenient in ambulatory settings as a single sample is required at 2h from feeding.

27
Q

What is the Dynamic test:

CGIT (Combined G-I test)?

A
  1. Fast overnight (12h)
  2. Obtain basal Glucose and Insulin
  3. 150mg/kg 50% glucose IV +0.1IU/kg soluble insulin IV (insulin <10 sec from glucose)
  4. Measure glucose at 1min, 5min then every 5 mint up until 45min, then every 15 minutes for 2-3 hours (17-20 samples in total)
  5. Measure insulin at 45 minutes
  6. Test convenient is expensive and time consuming but provides detailed information of insulin response to glucose challenge

Horses with IR will remain hyperglycemic for longer

28
Q

What is the In-feed glucose challenge?

A
  1. Fast overnight (12h)
  2. Administer non-glycaemic feed (chaff) with 1g/kg glucose powder orally
  3. Measure Insulin at 2h
  4. Insulin ≥ 85 IU/mL indicative of IR

Test convenient in ambulatory settings as a single sample is required at 2h from feeding.

29
Q

What are the treatments for EMS?

A

Management

  1. Diet

Reduce caloric intake

  • Reduce Starches in diet
  • Limit lush pasture grazing
  1. Exercise
  • Increase caloric consumption
  • Improves insulin sensitivity (skeletal muscle)
  • Increase glucose uptake from muscle

Pharmaceutical

Levothyroxin (used in SA as well, preparation from dogs given to horses effective to promote weight loss)

Metformin (promote weight loss)

30
Q

How should diet be managed to mange EMS?

A

Reduce starches in diet

  • Wash away hydrosoluble carbohydrates from hay
  • Start with 2%BWT as soaked hay, but lower to 1.5% if no weight loss in 6 weeks
  • Soak hay for at least 45 minutes (am for pm and viceversa)
  • Add balancer to reintegrate vitamins and minerals
  • Strictly no treats!!! Add signs to stable door!!!

Limit lush pasture grazing

  • Green grass unregulated source of sugars and starches
  • Short turn-out periods (<1h)
  • Small, bare paddock (tennis court)
  • Grazing muzzle
  • Co-graze with small ruminants
    • Supplement vitamin and minerals
31
Q

How should exercise be managed to manage EMS?

A
  • Burns calories and promotes weight loss
  • Promotes muscle insulin sensitivity
  • If active laminitis: No exercise until foot inflammation is under control. These cases are more challenging as rely solely on diet for weight loss
  • Intense exercise more effective
  • Mild or moderate exercise have little effect on insulin sensitivity
  • At least trot/canter for 30 min every day
  • Under saddle or on a long line
  • Increase work on hillsides

If exercise is really intense supplement diet, particularly if EMS is in lean phenotype

32
Q

How is levothyroxine used to treat EMS?

A

Levothyroxine

Not a substitute for diet, exercise, and management

Two indications:

  1. Short-term (3 to 6 months) treatment while responding to diet and exercise plan
  2. Refractory cases

Administer 0.1 mg/kg (48 mg/day for 500kg)

Increase to 0.15 mg/kg (72 mg/day) in extreme cases

Wean off gradually once target weight is reached

No equine formulation in the UK

Canine preparations cost prohibitive

33
Q

How does metformin treat EMS?

A

Increases insulin sensitivity enhancing glucose uptake in to cells

Inhibits gluconeogenesis and lipogenesis

Increases fatty acid oxidation and lipolysis

Blunted glycaemic and insulinaemic curve after oral dextrose challenge (30mg/kg PO)

No drug available for use in horses so need to use human drug

Variable and generally poor bioavailability

Administer fasted if possible (30-60 min before meal)

30mgkg PO BID

up to 50mg/kg PO TID if no improvement

More data necessary on potential tachyphylaxis

Some horses might show transient, mild signs of hypoglycaemia

34
Q
A
35
Q

Describe how Levothyroxine sodium works?

A
36
Q

Describe the drug metformin?

A

Equine Final Year (102 decks)

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