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Medicine III > Equine Endocrinology > Flashcards

Equine Endocrinology Flashcards

1
Q

Obj: Similarities & Differences between PPID & EMS

A
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2
Q

Obj: Pathogenesis of PPID & EMS

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3
Q

Obj: Role of dopamine in PPID

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4
Q

Obj: Equine Metabolic Syndrome

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5
Q

Obj: Insulin & its role in laminitis

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6
Q

Obj: Diagnostics and treatment of PPID & metabolic Syndrome

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7
Q

Obj: Importance of diet impact on insulin dysregulation (EMS)

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8
Q

What is the function of the Hypothalamus

A
  • Severs as a translator between the CNS and pituitary gland
  • Synthesizes releasing and inhibitory factors responsible for control of hormone release from the adenohypophysis and neurohypophysis
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9
Q

Why is Equine Pituitary Pars Intermedia Dysfunction (PPID) “Cushing’s” considered a hypothalamic disorder?

A

Primary hypothalamic disorder due to dopaminergic neurodegeneration

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10
Q

What are the parts of the Pituitary Gland?

A
  • Pars distalis
  • Pars intermedia
  • Pars nervosa & infundibular stalk
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11
Q

What is the function of the pars distalis?

A
  • Pleocelluar gland containing 5 cell types
    • Somatotrophs - growth hormone
    • lactotrophs - prolactin
    • Gonadotrophs - LH, FSH
    • Thyrotrophs - TSH
    • Corticotrophs - Pro-opiomelanocorticotropin (POMC)
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12
Q

How is POMC converted to ACTH

A

Post-translational processing by the prohormone convertase I

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13
Q

What is the function of the Pars Intermedia?

A
  • Homogenous cell population - melanotrophs
  • Contain prohormone convertase I & II
    • POMC is cleaved into α-MSH, β-endorphin, corticotrophin-like intermediate peptide (CLIP) and very little ACTH
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14
Q

How is the Pars intermedia controlled?

A
  • secretory control through tonic inhibition by dopamine w/ additional modulation by serotonin, β-adrenergic and gamma-aminobutyric acid (GABA) inputs
  • Dopamine in the pars is released directly from the nerve terminals - originate from periventricular nucleus of the hypothalamus
    • Interacts at the D2 receptors of the melanotrophes to decrease POMC production
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15
Q

What is the function of the pars nervosa and infundibular stalk?

A
  • composed of axons extending from nerve bodies in the hypothalamus and pituicytes
  • Oxytocin and ADH (vasopressin) are secreted from the axon terminals directly into circulation
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16
Q

What is the cause of Pituitary Pars Intermedia Dysfunction (PPID) in horses?

A
  • Hyperplasia or dysfunction of the pars intermedia results in excessive secretion proopiomelanocortin (POMC) by melanotropes
17
Q

What are the results of lack of dopaminergic innervation in the pars intermedia?

A
  • Hyperplasia and overproduction of POMC
  • Leads to increased production of:
    • β-endorphin
    • α-MSH (melanocyte stimulating hormone)
    • CLIP (corticotropin like peptide)
    • ACTH (adrenocorticotropin)
18
Q

What is the normal function of dopamine in the pars intermedia? How does PPID affect that?

A
  • Normally has a tonic inhibitory control over the pars intermedia
  • PPID - dopamine loss in the periventricular nuclei of the hypothalamus
19
Q

What are the clinical signs of PPID?

A
  • Due to:
    • Increased ACTH
    • Physical destruction of the pars nervosa
    • increased circulating concentrations of POMC-derived peptides
  • Usually Old horse (~20% of geriatric horses have PPID)
  • Long curly hair coat (hypertrichosis)
    • thick guard hairs
    • failure to shed in spring
    • early development of winter coat
  • Chronic laminitis
    • not all horses with PPID will have hyperinsulinemia & laminitis
  • Immunosuppression
  • PU/PD/PP
  • Hyperhidrosis
  • Excessive Cortisol - muscle wasting, hyperlipemia, insulin resistance, abnormal fat deposits, pendulous abdomen
20
Q

How is PPID diagnosed?

A
  • CBC - stress leukogram (matrue neutrophilia, lymphopenia)
  • Chem - hyperglycemia (150-350), hyperlipemia, mild elevations in liver enzymes
  • UA - glucosuria
  • Plasma ACTH concentration
    • catches Moderate/Advanced PPID
  • TRH stimulation
    • detects Early PPID
  • Overnight Dex Suppression
    • PPID fail to suppress endogenous cortisol after Dexamethasone
    • No negative feedback from pars intermedia
21
Q

What must be done with horse blood for Plasma ACTH concentration tests?

A
  • Plasma and blood must be separated within 3 hours of taking sample
22
Q

What is the treatment for Pituitary Adenomas?

A
  • Peroglide - FDA approved
    • Dopamine agonist (DA-2)
    • 0.5mg/500kg q24h
  • General treatments for improving insulin sensitivity
23
Q

What are the principle components of Equine Metabolic Syndrome?

A
  • Adiposity
    • abnormal fat deposits
  • Insulin resistance
    • dysregulation
  • Laminitis
    • clinical to subclinical
24
Q

What are the clinical signs/classis presentation of EMS?

A
  • Middle Aged
  • BCS >6, can be thin with abnormal fat deposits
    • Cresty neck, fat prepuce or mammary glands, fat in supraorbital fossa, above tail head
  • Mares - infertility
  • Laminitis - wide range - lameness, increased digital pulses, subclinical but divergent rings on feet, changes on radiographs (rotation of P3)
  • Hair coats are normal
25
Q

Why are EMS horses commonly diagnosed with hypothyroidism?

A
  • EMS horses have low circulating concentrations of thyroid hormones
    • glands and stimulation tests are normal
26
Q

What is the pathogenesis of Equine Metabolic Syndrome

A
  • Exact unknown
  • Diet:
    • Structural CHO - insoluble fiber in diet (cellulose, hemicelluloses, lingocellulose)
      • Fermented in the Large Colon
      • Good carbs
    • Non-structural Carbohydrates (NSC) - Sugar, starch, fructans
      • digested and absorbed in the small intestine
      • Insulin is produced in response
  • Genetics: anecdotal reports, “thrifty gene”
  • Exercise: lack of exercise → weight gain → insulin resistance
  • Hyperinsulinemia experimentally results in laminitis
27
Q

How is EMS diagnosed

A
  • Signalment and Phenotype
    • middle aged, obese, laminitic, w/ normal hair coat
  • Documentation of insulin resistance
28
Q

How is insulin resistance tested for in horses? how are results interpreted ?

A
  • Gold standard - difficult in clinical setting
  • Resting insulin concentration:
    • horse can eat hay (no grain/pasture)
    • Avoid stress or testing during concurrent illness/lameness
    • Glucose conc. are normal but high end
    • May not be sensitive in early cases
    • Useful for Positive diagnosis, but if insulin is not high, can’t rule out EMS
      • Resting insulin conc:
        • > 20umol/L = non-diagnostic
        • 20-50 umol/L = suspect if clinical signs present
        • >50umol/L = EMS
  • Oral Sugar Test:
    • Fast horse for 3-8hrs
      • administer light corn syrup (0.15ml/kg)
      • measure glucose and insulin conc at 60-90min
    • More sensitive than resting insulin concentration
    • Insulin >45umol/L = EMS
29
Q

How is EMS treated?

A
  • Goal - improve insulin sensitivity
    • Weight loss
      • Feed hay at 1.5-2% ideal body weight (15-20lbs for 1000lb horse)
    • avoid trigger foods
      • Avoid/limit pasture grass
        • especially during change/dynamic phase (spring, fall, heavy rain)
      • Feed hay with low NSC (<12%)
        • soaking in water reduce NSC by 50%
        • Grass hay generally best
      • In thin horses - feed more calories
        1. add fat - water soaked beet pulp, rice bran, corn oil
        2. Low-starch high fat diet
        3. feed smaller more frequent meals
    • exercise - daily, may be limited w/ laminitis
    • medication/supplements
      • Chromium 5-10mg
      • Thyroid Supplementation - for overweight EMS
        • weight loss and improved insulin sensitivity
        • 48 mg/horse for 3-6 months then wean off slowly
      • Metformin (dimethylbiguanide)
        • human diabetes type 2 drug - mixed results in studies
30
Q

What cuases dopaminergic neurodegeneration?

A
  • Accumulation of a misfolded protein
    • Alpha-synuclein - increase in nerve terminals
    • Related to oxidative stress
  • Chronic inflammation
  • Oxidative Stress
  • NOT a reduction in systemic anti-oxidant capacity
31
Q

How is the dopaminergic neurodegeneration in PPID horses similar to Parkinson’s in humans?

A
  • Motor dysfunction
  • Nigrostriatal neurons
  • Hormonal dysregulation
  • Periventricular hypothalamic neurons
32
Q

Why does laminitis develop?

A
  • Ischemic/Vascular theory
  • Mechanical/Traumatic
  • Metabolic/Enzymatic
33
Q

What syndromes are associated with Laminitis?

A
  • PPID & EMS
  • Corticosteroids
  • Systemic illness (Endotoxemia)
    • GI disease, retained placenta
  • Toxins - Black Walnut
  • Grain Overload
  • Idiopathic
34
Q

Why are horses with PPID PU/PD?

A
  • Hyperglycemia (Osmotic Diuresis)
  • Pars Nervosa - Destruction
    • lack of ADH
  • Cortisol - ADH interference
  • Cortisol increases GFR
35
Q

Why are horses with PPID PU/PD?

A
  • Hyperglycemia (Osmotic Diuresis)
  • Pars Nervosa - Destruction
    • lack of ADH
  • Cortisol - ADH interference
  • Cortisol increases GFR

Medicine III (32 decks)

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