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ENI2 > Equine endocrinopathies > Flashcards

Equine endocrinopathies Flashcards

1
Q

What is meant by Equine Metabolic Syndrome?

A

A collection of risk factors associated with an increased risk of laminitis

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2
Q

List the main risk factors in EMS

A
  • Obesity (which leads to…)
  • Insulin resistance (which leads to…)
  • Predisposition towards laminitis
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3
Q

List the potential additional components of EMS

A
  • Dyslipidaemia
  • Hypertension
  • Hyperleptinaemia
  • Altered reproductive cycling
  • Increased systemic markers of inflammation
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4
Q

Outline the epidemiology of EMS

A
  • Prevalence unknown
  • Age: 5-15yrs
  • Breeds: any breed but ponies, minis, Arabians, Warmbloods and native breeds are predisposed
  • Seasonal: spring-summer
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5
Q

Explain how season affects EMS

A
  • In Spring-summer, lush grass
  • Excess sugars produced in grass, converted to storage carbs e.g. fructans and starches
  • Taste good, higher calories = fat
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6
Q

Describe the appearance of obesity in a horse with EMS

A
  • Cresty neck
  • Pad pads in front and behind shoulder, hindquarters, belly fat, tail head
  • BCS >3.5/5
  • Fat in middle of neck
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7
Q

Explain how EMS might occur in lean horses due enzymatic action

A

11beta-hydroxysteroid dehydrogenase-1 is an enzyme that increases local production of cortisol in adipose tissue
- High cortisol = insulin resistance

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8
Q

Explain how EMS might occur in lean horses due to pancreatic disease

A

Pancreatic disease can result in reduced insulin production and thus type 2 diabetes mellitus

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9
Q

Describe the lameness commonly seen in EMS

A
  • Due to laminitis
  • Bilateral
  • Pottery gait, digital pulses, pain on coronary band
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10
Q

Describe the feet of a sound horse with EMS

A

Evidence of previous laminitis i..e divergent growth rings on hooves

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11
Q

List the elements of the pathophysiology of laminitis in EMS

A
  • Insulin resistance
  • Inflammation
  • Oxidative Stress
  • Altered adipocyte function
  • Altered endothelial function
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12
Q

What are the functions of adipose tissue?

A
  • Energy storage

- Hormone production

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13
Q

What hormones are produced by adipose tissue?

A
  • Adipokines (leptin, resistin, adiponectin, apelin)

- Adipocytokines (TNF, IL-1, IL-6)

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14
Q

What are the consequences of the hormones produced by adipose tissue?

A

Chronic low grade inflammation

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15
Q

How does insulin resistance occur in EMS?

A
  • Down regulation of insulin signalling by adipokines
  • Accumulation of intracellular lipids (lipotoxicity) e.g. in skeletal muscle cells, liver, pancreas (insulin would normally suppress lipolysis, without get more FFAs produced)
  • increased oxidative damage, altered insulin signalling
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16
Q

Describe the insulin and glucose levels in compensated insulin resistance

A
  • Normal glucose levels

- Hyperinsulinaemia

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17
Q

Describe the insulin and glucose levels in uncompensated insulin resistance

A
  • Hyperglycaemia

- Hyperinsulinaemia

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18
Q

Describe the insulin and glucose levels in type 2 diabetes mellitus

A
  • Hyperglycaemia (persistent)

- Hypoinsulinaemia

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19
Q

How might endothelial cell dysfunction occur in EMS?

A
  • Hyperinsulinaemia
  • Inhibition of NO release by endothelial cells
  • Endothelin-1 synthesis and sympathetic nervous activation
  • Glucose toxicity
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20
Q

Outline the processes that lead to laminitis in EMS

A
  • Hyperinsulinaemia leading to endothelial cell dysfunction
  • Digital vasoconstriction
  • Impaired glucose uptake from epidermal laminar cells
  • Altered epidermal cell function/mitosis
  • Matrix metalloproteinase activation
  • Pro-inflammatory/pro-oxidative state in lamellar tissue
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21
Q

What aspects of the history are important in the diagnosis of EMS?

A
  • Diet (quality and quantity)
  • Amount of exercise
  • Previous history of lameness
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22
Q

Compare diabetes mellitus in horses to that in other species

A
  • Rare in horses, when occurs often associated with PPID
  • Horses can remain hyperinsulinaemic for years without developing DM
  • No development of amylin within pancreas as seen with horses and cats
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23
Q

Outline the clinical relevance of hypothyroidism in horses

A
  • Very rare
  • Testing may involve SH stim but limited applicability, T3 and T4 of little use due to wide variation in normal horse
  • Affected by stress, disease, diet
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24
Q

What is meant by compensated insulin resistance?

A

Normal glucose concentrations maintained by increased insulin output, solved by weight loss

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25
Q

What is meant by uncompensated insulin resistance?

A

Glucose concentrations increasing and increased insulin to compensate for reduced effect (hyper-insulinaemia and glycaemia)

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26
Q

What is meant by type 2 diabetes?

A

Persistent hyperglycaemia and hypoinsulinaemia, end stage of insulin resistance

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27
Q

Why is EMS a risk factor for PPID?

A
  • Obesity and IR associated with low-grade inflammation and pro-oxidative state
  • Oxidative degeneration of dopaminergic neurons => PPID
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28
Q

What happens to insulin dysregulation with the development of PPID?

A

It is exacerbated

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29
Q

What are the aims of EMS diagnostic tests?

A
  • Confirm insulin resistance combined with clinical signs

- Rule out PPID

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30
Q

List the possible tests for EMS

A
  • Resting glucose and insulin
  • Proxies of insulin sensitivity
  • Dynamic testing e.g. CGIT
  • In feed glucose challenge
  • Blood pressure measurement
  • Adipokine measurement
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31
Q

Outline the use of resting glucose and insulin testing in the diagnosis of EMS (advantages, result interpretation, specificity/sensitivity)

A
  • Simple, cheap
  • High resting insulin strongly suggestive of IR
  • Low insulin and glucose = T2 DM
  • Low sensitivity and specificity (false negatives likely)
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32
Q

What factors may affect a resting glucose and insulin result?

A
  • Stress
  • Fed/fasted
  • Season (if at pasture)
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33
Q

Outline the method for an oral glucose challenge test

A
  • Fast overnight
  • Administer non-glycaemic feed (e..g chaff) with known amount of glucose powder (e.g. 1g/kg)
  • Measure insulin at 2hr
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34
Q

What result on an oral glucose challenge test would indicate insulin resistance?

A

At 2 hr insulin >95IU/ml

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35
Q

Outline the features of an oral glucose challenge test (advantages, disadvantages, additional)

A
  • Convenient in ambulatory settings
  • Better than basal insulin
  • Need to be organised and instruct owner to feed at a certain time, arrive and sample on time
  • Can also use a variation with sugar syrup rather than glucose powder
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36
Q

Describe the method for a combined glucose insulin test (CGIT)

A
  • Fast overnight
  • Obtain basal glucose and insulin
  • Give 150mg/kg glucose IV and immediately +0.1IU/kg soluble insulin (<10sec from glucose)
  • Measure glucose at 1 min, 5 min, then every 5 min until 45 min
  • Then measure every 15 min for 2-3 hours (17-20 samples total)
  • Measure insulin at 45 min
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37
Q

Outline the features of the CGIT (advantages, disadvantages, interpretation)

A
  • Provides detailed information of insulin response to glucose challenge
  • Expensive, time-consuming
  • Prolonged hyperglycaemia (above baseline within 30-45 mins) suggests IR, high insulin (>100IUml) at 45 min suggests exaggerated insulin response
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38
Q

Why does insulin higher than baseline >45 mins following CGIT suggest insulin resistance?

A

Insulin half life in the horse is only 40 mins

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39
Q

What are the 2 broad ways in which EMS can be managed?

A
  • Husbandry (including diet)

- Pharmaceutical

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40
Q

Give the key husbandry aspects in the management of EMS

A
  • Reduce caloric intake, starch in diet
  • Soak hay
  • Limit lush pasture grazing
  • Exercise increase
  • Laminitis management
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41
Q

Explain the soaking of hay in the management of EMS

A
  • Washes away hydrosoluble carbohydrates
  • Soak minimum 45 mins (most practical overnight/during day)
  • Add vitamin balancer
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42
Q

Explain the restriction of pasture grazing in the management of PPID

A
  • Green grass is unregulated source of sugars and starches
  • Best use small, bare paddock
  • Limit time outside <1h
  • Grazing muzzles
  • Co-graze with small ruminants
  • Supplement vitamins and minerals
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43
Q

Explain exercise in the management of PPID

A
  • Intense exercise most effective, 30min/day minimum (increase to this gradually)
  • Increase work on hillsides
  • Supplement diet if very intense or lean phenotype
  • Increases calorie use and improves insulin sensitivity
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44
Q

Outline the management of EMS with ongoing laminitis

A
  • Non exercise

- Manage entirely with diet

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45
Q

What drugs are used in the management of EMS?

A
  • Levothyroxine

- Metformin

46
Q

What are the 2 indications for the use of levothyroxine?

A
  • Short term use (3-6 months while wait for response to diet and exercise)
  • In refractory cases
47
Q

What are the actions of metformin?

A
  • Increase insulin sensitivity by increasing GLUT4 in membranes
  • Inhibit gluconeogenesis and lipogenesis (acctivate AMPkinase)- INcreased fatty acid oxidation and lipolysis
48
Q

What are some disadvantages of metformin?

A
  • Poor bioavailability

- Some horses may show mild signs of hypoglycaemia initially

49
Q

Describe the mechanism of action of levothyroxine

A
  • Synthetic form of thyroxine (T4) and acts as a metabolic stimulant
  • Increases basal metabolic rate
50
Q

What are the potential side effects of levothyroxine?

A
  • Mild hyperthyroidism

- Excitation

51
Q

What is the expected benefit of levothyroxine administration?

A

Reduced size of adipose deposits

52
Q

What monitoring is required when using levothyroxine?

A
  • Total T4 concentrations

- Signs of hyperthyroidism (tachycardia, polyphagia, excitability, nervousness, panting)

53
Q

What is the approximate cost of levothyroxine treatment for 1 month?

A
  • Expensive

- 0.1mg/kg -> £10-15/day

54
Q

What are the potential side effects of treatment with metformin?

A
  • Oral irritation/ulceration
  • Metabolic acidosis (in other species)
  • (Colic, severe respiratory problems also noted)
55
Q

What is the expected benefit of treatment with metformin?

A

Blunts post-prandial hyperglycaemia and hyperinsulinaemia => reduces the risk of laminitis

56
Q

What monitoring is required with metformin treatment?

A

None

57
Q

What is the approximate cost of metformin treatment for 1 month?

A

~£15 for a 500kg horse

58
Q

Describe the signalment of PPID

A
  • > 7yo, average 19-21yo/15yo
  • No gender predilection
  • Ponies predisposed
59
Q

In a horse, what would the following clinical signs be indicative of?

  • Weight loss, muscle wastage
  • PUPD
  • Hirsutism
  • Quieter demeanour
  • Lethargy
  • Poor performance
  • Potbelly
  • Chronic laminitis
  • Recurrent infection
A 
- PPID
May also see (rare):
- hyperhidrosis/anhydrosis
- Neurologic (blindness, seizures, narcolepsy)
- Absent reproductive cycle/infertility
60
Q

What areas are prone to adiposity in PPID vs EMS?

A
  • Supraorbital area

- Tail base, shoulder blade and neck more common in EMS

61
Q

Where is ACTH normally produced in the horse?

A

The pars distalis of the anterior pituitary gland, and very small amounts from the pars intermedia

62
Q

What is ACTH normally released in response to?

A

Stressful situations e.g. pain, illness, excitement, exercise, travel

63
Q

What leads to the hormonal changes that occur in PPID?

A
  • Lack of dopaminergic inhibition of the pars intermedia

- Hyperplastic/neoplastic changes with functional cells of the pars intermedia

64
Q

What metabolic factor leads to the loss of dopaminergic inhibition in PPID?

A

Oxidative damage due to obesity

65
Q

How does loss of dopaminergic inhibition lead to PPID?

A
  • Dopaminergic neurons are inhibitory
  • Loss of these leads to loss of inhibition of melanotropes
  • Melanotropes become hyperplastic and increase hormone secretion = functional pituitary adenomas
66
Q

Name the hypothalamic tracts and identify which one is involved in pars intermedia activity

A
  • Tuberoinfundibular, tuberohypophyseal, periventricular

- Periventricular is involved in PI activity

67
Q

Explain why EMS is a risk factor for PPID

A
  • Obesity and insulin resistance lead to low grade inflammation, pro-oxidative state
  • Increases oxidative degeneration of dopaminergic neurons
  • PPID develops earlier in horses with EMS
68
Q

Briefly outline pituitary independent Cushing’s syndrome in horses

A
  • Primary adrenocortical tumours rare in horses and usually non-functional
  • Not worth considering as part of differentials
69
Q

How do the hormonal imbalances in equine Cushing’s lead to weight loss and muscle wastage?

A
  • Loss of abdominal muscle mass/strength and heavy viscera = rounded appearance
  • Hypercortisolaemia = increased gluconeogenesis and protein catabolism
70
Q

How do the hormonal imbalances in equine Cushing’s lead to PUPD?

A
  • Hypercortisolaemia = increased GFR, reduced ADH, increased water loss
  • Hyperglycaemia leads to osmotic diuresis
  • Neurogenic diabetes insipidus due to compression of pars nervosa from adenoma of pars intermedia (less ADH)
  • Increased water loss through hyperhydrosis
71
Q

How do the hormonal imbalances in equine Cushing’s lead to hirsutism?

A
  • Lack of decrease in MSH (normally occurs in spring)
  • Lack of rise in prolactin which triggers shedding
  • Hair held in telogen phase due to increased MSH
72
Q

How do the hormonal imbalances in equine Cushing’s lead to lethargy?

A
  • Increased beta-endorphins in plasma and CSF

- Increased tolerance to pain and lethargic demeanour

73
Q

How do the hormonal imbalances in equine Cushing’s lead to increased risk of chronic laminitis?

A

Hypercortisolaemia increases insulin resistance, leading to hyperinsulinaemia (causes laminitis alone) and hyperglycaemia (glucose toxicity can also lead to laminitis)

74
Q

How do the hormonal imbalances in Cushing’s lead to increased susceptibility to disease?

A

Hypercortisolaemia leads to immunosuppression and reduced neutrophil function

75
Q

How do the hormonal imbalances in equine Cushing’s lead to poor fertility?

A
  • Increased size of pituitary gland leading to destruction of gonadotrophs of anterior pituitary and suppression of gonadotrophin by glucocorticoids and androgens produced by adrenal cortex
  • Leads to abnormal oestrus activity and oestrus suppression
76
Q

What tests are required for diagnosis of PPID?

A
  • Haematology
  • Biochemistry
  • Resting ACTH concentration
  • TRH stimulation test
77
Q

What haematology and blood biochem results would be expected in a horse with PPID?

A
  • Anaemia
  • Neutrophilia/lymphopaenia (stress leukogram)
  • Hyperinsulinaemia
  • Hyperglycaemia
  • Hyperlipaemia
  • High liver enzymes
  • Glucosuria
78
Q

What can an oral glucose test be used for?

A

Ruling OUT EMS and to assess insulin sensitivity status in a horse with PPID

79
Q

Is a resting ACTH test better for ruling in or out PPID?

A

Ruling in, it has a low sensitivity so false negatives are likely

80
Q

Describe the processing of a resting ACTH test

A
  • Submit EDTA plasma
  • Needs to be separated and refrigerated within 3 hours of collection as ACTH degenerates at room temperature
  • Samples must be submitted chilled
81
Q

What may lead to a false positive on resting ACTH?

A
  • Freezing full blood

- Stress e.g. pain, infections, hospitalisation, transport

82
Q

Describe the results expected in a PPID positive animal in Autumn or Summer

A
  • Autumn (Aug, Sept, Oct): >47pg/ml

- Summer: >29pg/ml

83
Q

Outline the TRH stimulation test for PPId

A
  • Inject 1.0mg thyrotroping releasing hormone IV at T0
  • take samples at 0mins and at 10 mins (+/- 30 mins sample)
  • Should stimulate release of ACTH from PI
84
Q

Outline the seasonality of TRH stimulation testing

A

Should avoid testing August to September (sensitivity 77%, specificity 82%)

85
Q

What is TRH stimulation best used for?

A

Ruling out PPID in early suspicion cases i.e. cases with borderline elevated resting ACTH

86
Q

What results on a TRH stimulation test would be expected in a PPID positive patient?

A
  • At T0: ACTH >35pg/ml

- At T10: ACTH >110pg/ml

87
Q

Outline the dexamethasone suppression test

A
  • Historical, rarely used now

- Inject 0.04mg/kg dex IV or IM, measure cortisol at 19-24h

88
Q

What is the sensitivity and specificity of the dexamethasone suppression test for PPID?

A
  • Sensitivity: 65% or less

- Specificity: 76-100%

89
Q

What results would be expected on a dexamethasone suppression test in a horse with PPID?

A

Failure to suppress below 2nmol/L

90
Q

Outline process for the combined DST and TRH stimulation test for PPID

A
  • Dex 40ug/kg IV at 8-10am
  • Then TRH 1mg IV 3.5h after dex
  • Collect blood at 0h, 3h, 3.5h, 24h
  • More samples, more time consuming, more expensive
91
Q

Describe the sensitivity and specificity of the combined DST/TRH stimulation test

A
  • Increased sensitivity for early PPID cases

- Sensitivity 88%, specificity 76%

92
Q

What results would be expected in the combined DST/TRH stimulation test in a horse with PPID?

A
  • ACTH > 27nmol/l at 24 h

- Or greater than 66% increase between 3h and 3.5h (post TRH addition) sample

93
Q

What are the treatments available for the treatment of equine Cushing’s disease?

A
  • Pergolide (dopamine agonist)
  • Cyproheptadine (serotonin antagonist)
  • Chasteberry/Vitex agnuns castus
  • Trilostane
  • Diet management
  • Laminitis management
  • Antimicrobials
  • Vit E supplementation
94
Q

What is the mechanism of action of pergolide?

A
  • Dopamine receptor agonist

- Replaces the dopamine inhibition of melanotrophs

95
Q

How is ACTH produced and why does this lead to increases in other hormones in PPID?

A
  • Melanotrophs produce POMCs
  • Cleaved by prohormone convertase 1 to produce ACTH
  • POMCs further cleaved to produce MSH, beta-endorphins, CLIP
  • Loss of inhibition leads to increased production of all POMC derived hormones
96
Q

What are the potential side effects of pergolide?

A
  • Transient anorexia and lethargy
  • Mild CNS signs (mild depression, mild ataxia)
  • Diarrhoea, colic, sweating
97
Q

What monitoring is required while treating a horse using pergolide?

A
  • Plasma ACTH concentration

- Or TRH stimulation tests

98
Q

Give the approximate cost of a month of pergolide treatment in a 500kg horse

A

~£30

Pack of 60 = £70, pack fo 160= £140

99
Q

Outline the dosing regime for pergolide

A
  • First start at 1mg total q24h by mouth
  • If no improvement at first 4-6 week interval increase by 0.5mg/kg
  • Maximum dose 5mg total/d1ay
  • Each tablet 1mg
100
Q

What is the mechanism of action of cyproheptadine?

A

Serotonin antagonist

101
Q

Describe the dosing regime with cyproheptadine

A
  • Only in combination with pergolide
  • 0.25mg/kg PO q24h for 2 weeks
  • Then increase to q12h
  • 125mg for 500kg horse
102
Q

Give the approximate cost of treatment using cyproheptadine

A

4mg = 1 tablet = 4pence at whole sale/7pence at retail

103
Q

What side effects may occur with cyproheptadine treatment?

A
  • Drowsiness

- Ataxia

104
Q

What are the expected benefits of treatment with pergolide?

A
  • Initial improvement in attitude
  • Then improvement in PUPD
  • Then improvement in muscle mass and haircoat
105
Q

Outline the use of Trilostane in the treatment of equine Cushing’s

A
  • Some subjective clinical improvement
  • Older studies found no improvement
  • Currently not recommended
106
Q

Outline the use of vitex agnus castus in the treatment of equine Cushing’s

A
  • Herbal product (aka Chasteberry)

- Supposedlystimulates dopamine receptor activity but no positive effect found in studies

107
Q

Outline the dietary management of a PPID patient

A
  • Adequate caloric intake
  • Consider insulin sensitivity status
  • Free choice hay (2%BWT)
  • OIl to supplement calories (1-2 cups daily)
108
Q

Outline the management of laminitis in a PPID patient

A
  • NSAIDs

- Farriery (choose experienced farrier)

109
Q

Outline the use of vitamin E supplementation in the management of PPID

A
  • Little evidence, but may prevent further oxidative damage

- Costly

110
Q

Why are regular faecal egg counts and dental examinations advised for PPID patients?

A
  • Immunosuppression

- Increased risk of dental infection and GI parasitism

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