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Endocrinology > Equine Endocrine Disease > Flashcards

Equine Endocrine Disease Flashcards

1
Q

Pituitary Pars Intermedia Dysfunction (PPID)

A
  • Hairy horse, most common endocrinopathy
  • dopamine from hypothalamus controls melnotrops
    • disruption of dopamine = too much ACTH and cortisol
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2
Q

Pituitary gland

A
  • Three distinct lobes
    • Pars distalis
    • Pars intermedia
    • Pars nervosa
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3
Q

Pars intermedia

A
  • melanotrop => proopiomelancortin (POMC)
    • POMC =>
      • alpha - MSH
      • beta - Endorphin
      • corticotrophin - like intermediate lobe peptide (CLIP)
    • some ACTH
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4
Q

Pars distalis

A
  • Corticotrophs => different POMC peptides than PI
    • POMC => ACTH
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5
Q

Positive control of melanotrophs

A
  • controlled by THR
    • which releases MSH (this increases in the fall-prep for winter)
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6
Q

Dysfunction of Pars Intermedia

A
  • Loss of dopaminergic inhibition of PI
  • Neurons in hypothalamus degenerate = dec dopamine conc
    • => neurodegeneration root cause
  • Pars intermedia enlarges => compresses remaining gland structures
  • hypertrophy => hyperplasia => adenoma formation
    • benign hyperplastic process
    • secretes a small amount of ACTH (more than a normal horse)
      • POMC derived peptides accentuate actions of ACTH
        • => more cortisol made by adrenal gland
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7
Q

Etiology PPID

Clinical Signs

A
  • Etiology
    • Older horses more likely to acquire PPID
  • Clinical Signs
    • Hirsutism (long curly hair that fails to shed)
    • PU/PD
    • Laminitis
    • Muscle wasting/weight loss
    • Bulging eyes/perioorbital swelling
    • hyperhidrosis (even clipped)
    • Immunospuression (skin eye inf, subsolar abscesses, sinusitus)
    • Inc apetite
    • lethargy
    • blindness
    • infertility
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8
Q

Early Clinical Signs PPID

A
  • Delayed haircoat shedding
  • Shift in metabolism
  • Regional adiposity
  • +/- Fertility problems
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9
Q

PPID Diagnostic testing

A
  1. HIRSUTISM
  2. Endogenous ACTH
  3. Dexamethasone Suppression Test
  4. TRH stimulation test
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10
Q

Things that later ACTH concentration

A
  • EVERYTHING
  • Stress
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11
Q

Dexamethasone Suppression test

A
  • ACTH secreted by PI doesn’t respond to normal feedback in PPID
  • exogenous steroids don’t reduce cortisol production
  • Antemortem ‘gold standard’
  • requires 2 farm visits (overnight test)
  • misses early cases
    • not 100% sensitive/specific
  • perceived risk of laminitis
  • seasonal variations
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12
Q

Endogenous ACTH

A
  • morning, single blood draw
  • seasonal effect
  • less sensitive than DST
  • EDTA tube, spin down, ship on ice, sample good for 12 hours
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13
Q

TRH Stimulation Test

A
  • Admin TRH (I mg IV), then take blood sample to measure ACTH
    • affected horses: sig inc ACTH and cortisol (45-90 min post adm)
  • Can also measure a MSH respones to TRH stim
  • Avoids conplications from dexamethasone admin
  • TRH available as compounded med
  • needs to be validated in larger pops and in fall
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14
Q

Other PPID tests

Tests that aren’t accurate

A
  • Other tests
    • screen for insulin resistence in PPID positives
  • Not useful
    1. single/multiple cortisol conc (too many other things affect this)
    2. Diurnal ‘cortisol rhythm’ concentrations
    3. Urinary cortisol:creatinine ratio
    4. Insuline concentration
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15
Q

PPID Treatment

Goal

Drugs

A
  • Goals: increase dopaminergic control of pituitarty
    1. Reduce or minimize clinical signs
    2. Avoid laminitis / founder
    3. Dx and manage insulin resistence
    4. Improve fertility…?
  • Drugs
    • Dopamine agonists
    • Serotonin antagonists
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16
Q

PPID treatment with Pergolide

A
  1. Pergolide: dopamine agonists (1 mg/horse)
    • now available as Prascend
  2. Assess response in 30 days
  3. Primary side effects
    • depression
    • anorexia
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17
Q

PPID treatment with Cyproheptadien

A
  • Cyproheptadine: serotonin antagonist
    • goal to block ACTH production from PI
    • Inconsistent response
    • 0.5 mg/kg 1-2 times daily
    • may improve clinical signs
    • can be used as adjuct to pergalide
18
Q

Managing PPID

A
  • 35-45 $ per month (not everyone will treat)
  • Clipping hair
  • manage feed (trims, rads, therapeutic shoeing)
19
Q

Equine Metaboilc Syndrome (EMS)

Case definition

A
  • Insulin resistance
  • Obesity and/or regional adiposity
  • Prior or current lamiitis
  • ‘easy keeper’
  • Laminitis assoc with spring grass
20
Q

EMS predisposition

A
  • Metabolically thrifty horses
    • ponies, morgans, Pasos, Norweigian Fjords
  • Aged 5-20 yo
  • Most are obese
21
Q

Prolonged hyperinsulinemia

A
  • Will induce laminitis
22
Q

EMS Diagnostic testing

A
  1. Resting Insuline/Glucose concentration
    • do in the morning w/o access to sugars/food
    • make sure horse isn’t stressed
  2. Oral Glucose Tolerance Tests
    • give oral light karo syrum, draw blood 60-90 minutes later
    • high glucose (>115 mg/dL) and insulin (>60 mic/mL) positive for IR and EMS
  3. Combined Glucose - Insuline Test (can cause hypoglycemia)
    • takes about 3 hours
23
Q

Horses with an insuling level > 100

A
  • risk foundering immediately this second!
24
Q

Goals of treatment EMS

A
  • Improve insulin sensitivity => inc threshold for laminitis
  • Reduce body fat (adiposity inc insulin resistence)
  • Avoid high starch/sugar feeds
  • Exercise, if possible
25
Q

Managing obesity

A
  • cut forage to 1.5 % BW in hay
  • slowly reduce to 1.5% ideal body weight
  • Choose hay < 10% Non-structural carbohydrate
    • get crappy hay
    • or soak hay for 30 min (leaches out carbs)
  • Restrict pasture access (1-2 hours a day)
  • Grazing muzzle
26
Q

Pharmacologic approaches to managing EMS

A
  1. Levothyroxine (weight loss strategy)
    • short term therapy at very high dose, must wean off
  2. Metformin
    • not super commin, given at meals
  3. Corticosteroids
    • associated with laminitis…?
    • worse in IR horses…?
27
Q

Thyroid dysfunction

A
  • Hypothyroidism does not exist in horses
28
Q

Euthyroid Sick Syndrome

A
  • aka: non-thyroidal illness syndrom
  • changes in thyroid function occur with systemic disease
    • dec metabolic rate and preserve body mass…?
  • recognized in
    • humans and dogs
    • amount of suppression correlated with severity of dz
29
Q

Calcium homeostasis

A
  • most regulation in Equine GI system
  • most Ca and P found in teeth and bones
  • 50% plasma calcium is ionized
  • 40% plasma calcium bound to protein
  • 5-10% plasma calcium bound to citrate, nitrate and sulfate
  • alkalemia => low ionized Ca
  • acidosis => inc ionized Ca
30
Q

Hormones in Ca homeostasis

A
  • PTH => inc plasma Ca
    • bone, kidney
  • Calcitriol (vit D3) => inc plasma Ca
    • intestine
  • Calcitonin => decreases plasma Ca
    • bone
31
Q

Conditions associated with Hypocalcemia

A
  • Synchronous diaphragmatic flutter: thumps
  • Lacation tetany
  • Seizures
  • Colic-endotoxemia
32
Q

Synchronous Diaphragmatic Flutter

SDF

A
  • Depolarization of the phrenic nerve occurs in time with right atrium
    • stimulates contraction of diaphragm
  • Clinical Sign of hypocalcemia
  • thoracic/flank musculature contractions ‘ticking’ in time with HR
    • thumping noise
  • horse usually very anxious
  • Clin path
    • Low Ca, metabolic alkalosis, low K, Na
    • alkalosis contributes to hypoCa
    • Mg may also be decreased
  • TX: give Ca and solve whatever caused hypocalcemia to begin with

*horse specific

33
Q

Lactation Tetany

A
  • anytime from pre-foaling to post-weaning
  • Profuse sweating, anxious
  • stiff gain, muscle fasiculations
  • Tachycardia/arrhythmia
  • Colic w/unremarkable rectal, ileus
  • Clin path: dec ionized Ca
34
Q

Sepsis/Endotoxemia/Colic

A
  • common cause of hypoCa in hospital
  • Insufficient PTH secretion and intracellular Ca sequestration
35
Q

Blister beetles

A
  • causative agent of hypocalcemia
  • reported regularly in FL
  • found in alfalfa hay
  • Canthardin
    • vesicant
    • highly irritating
    • absorbed in GI and excreted in urine
    • GI and renal irritation, muscle damage
    • dose dep (1 beetle enough)
36
Q

Blister beetle tox Clinical Signs

A
  • Fever
  • Tachycardia/pnea
  • PD, dehydration
  • Hematuria

Due to HypoCa:

  • Muscle fasciculations
  • Sweating
  • Arrhythmias
  • SDF
37
Q

Hypercalcemia

A
  1. Primary/Secondary hyperparathyroidism
  2. Hypervitaminosis D
38
Q

Secondary Nutritional Hyperaparathyroidism

A
  • Dec Ca intake or excessive ingestion of P, oxalates
  • Stimulates PTH
  • CA and P mobilize from bone
  • Bone replacedment by fibrous connective tissue
    • over months
39
Q

Secondary Nutritional Hyperparathyroidism

History/CS/DX

A
  • History
    • Diet low in Ca, high in PO4 (Bran disease)
  • CS
    • ‘big head’
    • Bones of maxilla widen
    • loosening of teeth
    • shifting leg lameness
    • pathological fractures
  • DX
    • history
    • PE
40
Q

Secondary Nutritional Hyperparathyroidism

treatment

A
  1. inc Ca, dec P in diet
  2. Ca:P ratio 4:1 to induce remission
    • alfalfa
    • Calcium carbonate
    • can take 9-12 months for recovery

*normal diet: Ca:P ratio of 1:1 - 2:1

41
Q

Anhidrosis

A
  • Catecholamines => sweat glands => sweat
  • Etiology of acute dz unknown
  • No known predilection
42
Q

Annhidrosis

Chronic signs/DX/TX

A

Chronic signs

  • Alopecia on forehead
  • Poor performance
  • dry flaky skin
  • dec water consumption

DX

  • Clinical dx, terbutaline sweat test if someone doesn’t believe dx

TX

  • change environment or keep cool

Endocrinology (13 decks)

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