Endocrine Disease - Equine Flashcards

1
Q

What is the pathogenesis of hyperlipidemia?

A

negative energy balance

  • triggers excessive mobilization of fatty acids from adipose tissue
  • increased hepatic triglyceride synthesis and secretion of low density lipoproteins
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2
Q

What is hyperlipidemia?

What is hyperlipema?

A

hyperlipidemia - increased amount of all lipids and serum triglycerides (TG < 500 with clear plasma)

hyperlipemia - serum TG > 500 with cloudy serum

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3
Q

What are the risk factors for hyperlipidemia?

A
  • ponies, miniature horses, donkeys
  • obesity
  • stress
  • pregnancy
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4
Q

Describe the actions of the hormones involved in fat mobilization

A

lipoprotein lipase - activated by insulin, favors TG accumulation in adipose tissue

hormone sensitive lipase - expressed in adipose tissue, mobilizes stored fats
- inhibited by insulin

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5
Q

What are the 3 components of equine metabolic syndrome?

A
  • increased adiposity (fat depositions)
  • hyperinsulinemia
  • insulin resistance
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6
Q

Which breeds are predisposed to equine metabolic syndrome?

A

ponies and Morgans

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7
Q

What is the biochemical cause of hyperlipemia?

A

overproduction of triglyceride

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8
Q

What are the complications associated with hyperlipidemia?

A
  • hepatic failure
  • renal failure
  • death
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9
Q

What are the possible clinical presentations of equine metabolic syndrome?

A
  • generalized obesity
  • regional adiopsity
  • laminitis
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10
Q

What is compensatory insulin resistance?

A

production of higher levels of of insulin, trying to overcome the resistance
- will be hyperinsulinemic

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11
Q

What is non-compensatory insulin resistance?

A

pancreatic insufficiency develops due to beta cell exhaustion

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12
Q

How is equine metabolic syndrome diagnosed?

A
  • cresty neck
  • fasting insulin levels
  • insulin tolerance test
  • oral sugar test
  • combined glucose insulin test
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13
Q

Describe the insulin tolerance test

A
  • insulin is administered and glucose concentration is measured over time
  • normal if the concentration of glucose decreases by 50% within 30 minutes
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14
Q

Describe the Oral Sugar test

A
  • fast the horse overnight
  • administer corn syrup orally
  • collect blood at 60 and 90 minutes
  • measure insulin concentration
    (> 60 at either time indicates post-prandial hyperinsulinemia)
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15
Q

Describe the combined glucose insulin test

A
  • collect baseline blood sample, then IV infusion of dextrose followed by insulin
  • if insulin resistant: BG concentrations remaining above baseline for > 45 minutes
  • stress can alter results
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16
Q

What is the treatment for equine metabolic syndrome?

A
  • increase activity and weight reduction
  • limit sugars and carbs
  • restrict pasture access
  • Levothyroxine sodium, Metformin, Metaborol
17
Q

What are the 3 types of hypothyroidism?

A

primary - iodine deficiency or excess

secondary - pituitary or hypothalamic dysfunction

tertiary - defect of hormone use at the periphery

18
Q

What are the clinical signs associated with hypothyroidism?

A
  • weight loss
  • decrease in temp, HR, and CO
  • increased sensitivity to cold
  • lethargy, limb edema, decreased appetite
19
Q

How is hypothyroidism diagnosed?

A
  • baseline T3-T4
  • T4 radioimmunoassay (most reliable)
  • TRH or TSH stimulation test
20
Q

How is hypothyroidism treated?

A

Levothyroxine supplementation

21
Q

What is melanocyte stimulating hormone?

What are its functions?

A
  • a primary product of POMC cleavage
  • role in metabolism and obesity
  • anti-inflammatory hormone
  • reduces neutrophilic oxidative burst, chemotaxis, and adhesion
  • antipyretic
22
Q

What is the function of ACTH?

A

stimulates the adrenal glands to produce large amounts of cortisol

23
Q

What are the functions of cortisol?

A
  • stimulates gluconeogenesis
  • activates anti-stress and anti-inflammatory pathways
  • counteracts insulin
  • diuretic, increases GFR, Na retention, and K secretion
24
Q

What is the pathophysiology of Equine Pituitary pars Intermedia Dysfunction?

A
  • a neurogenerative disease with loss of dopaminergic inhibitory input to the melanotropes of the pars intermedia
  • hyperplasia of the pars intermedia
  • slow progressive disease
25
Q

What are the signs associated with PPID?

A
  • hirsutism
  • behavioral abnormalities
  • muscle atrophy (epaxial and gluteal)
  • abnormal fat distribution
  • PU/PD
  • hyperhidrosis
  • infertiliy
  • neurologic disease
  • laminitis
26
Q

How is PPID diagnosed?

A
  • plasma ACTH concentration
  • Dexmethasone suppression test
  • MSH plasma concentration
  • Domperidone stimulation test
  • ACTH stimulation test
  • TRH stimulation test
  • combined DST and TRH stimulation test
27
Q

What are the treatments for PPID?

A
  • Peroglide (dopamine agonist)
  • Cyproheptadine
  • Trilostane