Equine Endocrine/metabolic Conditions

Front 1

What individuals are susceptible to hyperlipemia?

Back 1

ponies, donkeys, mini horses, late preg or lactating, overweight horses

Front 2

What is hyperlipemia & what is the pathogenesis?

Back 2

plasma lipids > 500 mg/dl

triggered by any disorder that causes neg. energy balance --> ↑ fat mobilized from adipose to liver --> fat accumulates in liver or goes into plasma

Front 3

What are the clinical signs of hyperlipemia?

Back 3

anorexia, depression, weakness --> muscle fasciculations, ataxia, end stage recumbency
+/- diarrhea, +/- ventral edema

Front 4

How is hyperlipemia diagnosed?

Back 4

lipemic plasma, ↑ plasma TG (>500 mg/dl), liver enzyme & function tests

Front 5

What is the tx for hyperlipemia?

Back 5

tx underlying dz

improve energy balance: ↑ BG to ↓ mobilization of fat (glucose, +/- insulin, +/- heparin)

hydration

Front 6

What is nutritional secondary hyperparathyroidism?

Back 6

bone demineralization 2º to stimulation of PTH release by dietary Ca def. or dietary P excess (slowly progressive)

Ca/P imbalance --> ↑ PTH, ↑ active vit. D, Ca & P resorption from GI & bone

Front 7

What are the clinical signs of nutritional secondary hyperparathyoridism?

Back 7

“poor doer”, lameness, stiff gait, loose tooth, abnormal mastication, head enlargement, thickening of mandibles & nasal bones

Front 8

How is nutritional secondary hyperparathyroidism diagnosed?

Back 8

dietary hx
rad evidence of demineralization
normal serum Ca & P
↑ fractional excretion of P (conclusive: > 4%, suspected > 0.5%)
↑ PTH

Front 9

What is the tx for nutritional secondary hyperparathyroidism?

Back 9

Ca supplement: limestone, alfalfa hay

confinement until bone density is normal

+/- NSAIDs for pain

Front 10

What are some causes of hypocalcemia?

Back 10

lactational demands
alkalemia
urea poisoning
blister beetle poisoning
pancreatic atrophy
corticosteroids
endotoxemia (↑ procalcitonin, perhaps an inflamm. cytokine)

Front 11

What individuals are prone to developing hypocalcemia?

Back 11

ponies, donkeys, mini horses, late preg or lactating

Front 12

What are some clinical signs of hypocalcemia?

Back 12

depression or anxiety, colic, thumps, tachypnea, tachycardia, ↓ sensory awareness, stiff gait, abnormal facial expression, elevation of tail head, muscle fasciculations, tremors, profuse sweating, dysphagia, laryngospasm, salivation, bruxism, tetany, ataxia, recumbency, stupor

Front 13

What is the tx for hypocalcemia?

Back 13

mild: oral limestone, alfalfa hay

moderate to severe: IV calcium gluconate (monitor HR & sounds: stop if bradycardia or arrhythmia develops)

Front 14

What is synchronous diaphragmatic flutter ("thumps")?

Back 14

hyperirritability of phrenic nerve caused by electrolyte imbalances (hypocalcemia, alkalemia) --> twitching in flank region, synchronous w/ heart beat (a symptom, not a dz)

Front 15

What is the tx for thumps?

Back 15

oral or IV Ca

Front 16

What is the pathogeneis of anhidrosis?

Back 16

inability to sweat in response to appropriate stimuli

cause unknown: affected horses have atrophied sweat glands
main theory: irregularity of neuronal control of sweat glands

Front 17

What are the clinical signs of anhidrosis?

Back 17

exercise intolerance, tachypnea --> panting, failure to sweat, ↑ body temp, poor haircoat (if chronic)

Front 18

How is anhidrosis diagnosed?

Back 18

hx & PE

“lunge test” (most sensitive): affected horses continue to have ↑ RR 30 min. after trotting for 30 min.

“sweat test”: intradermal inj. of terbutaline or epi, affected horse won’t sweat

Front 19

What is the tx for anhidrosis?

Back 19

cool environment
↓ stress & exercise
make sure horse is fit before hot weather starts
work horse during cool parts of day
feed high fat diet
electrolyte supplements
tyrosine supplement?

Front 20

What physical attributes &/or syndromes have traditionally been assoc. w/ hypothyroidism in adult horses?

Back 20

traditionally assoc. physical attributes: obesity, wt. gain, fat cresty neck, chronic laminitis

traditionally assoc. syndromes: laminitis, recurrent rhabdomyolysis, infertility in mares, anhidrosis, alopecia

Front 21

What are some physiologic or pathologic influences on thyroid function?

Back 21

NSAIDs, corticosteroids, high energy or protein diets, high Zn or copper levels in diet, food deprivation, high intensity exercise

Front 22

What are some problems w/ thyroid testing in horses?

Back 22

single measurements of thyroid hormones difficult to interpret: physiologic or pathologic influences

many labs don’t offer measurement of free fractions of thyroid hormones

stimulation tests (TRH, TSH) superior to single measurements of resting thyroid hormone concentrations: prohibitively expensive & impractical or unavailable to many clinicians

no commercially available assay for equine TSH

Front 23

How is hypothyroidism presumptively diagnosed?

Back 23

low serum free T4, T3
suggestive clinical signs
R/O non-thyroidal factors

Front 24

What is the tx for hypothyroidism?

Back 24

L-thyroxine, iodinated casein, triiodothyronine

Front 25

What is the cause of congenital goiter?

Back 25

ingestion of goitrogenic plants or ingestion of too much or too little iodine by dam during gestation

Front 26

What are clinical signs of goiter in foals?

Back 26

visible goiter
weak, poor doers: incoordination, hypothermia, poor suckling reflex, poor righting reflexes

Front 27

What is the pathogenesis of equine metabolic syndrome?

Back 27

insulin insensitivity --> hyperglycemia & glucotoxicity or intracellular glucose starvation

mechanism not well understood: domesticated horses eat more excess carbs, more sedentary?

Front 28

What are the clinical signs of equine metabolic syndrome?

Back 28

“easy keeper”: gain wt. easily, overweight, cresty neck, laminitis

Front 29

What are some factors that influence insulin sensitivity?

Back 29

sex, diet, age, exercise, pregnancy, stress, obesity, dz states (PPID, hyperlipemia, laminitis), breed?

Front 30

How is equine metabolic syndrome treated?

Back 30

avoid obesity/wt. reduction

less food: do not cut TOO much or TOO fast: risk of ↑ insulin resistance or hyperlipemia
low glycemic index
feed grass hays (not > 10% sugar & starch combined at 1.5-2% of TARGET BW)

↑ physical activity

Front 31

What is the pathogenesis of PPID?

Back 31

↓ in hypothalamic inhibitory control of pars intermedia of pituitary gland --> hypertrophy, hyperplasia, & microadenomas

degeneration of periventricular hypophyseal dopaminergic neurons --> PPID

Front 32

What are the clinical signs of PPID?

Back 32

long shaggy haircoat w/ delayed shedding
hyperhidrosis (↑ greasy sweat)
PU/PD
muscle atrophy

Front 33

What are some common complications of PPID?

Back 33

laminitis
wounds that don’t heal
chronic respiratory infections
dental dz
sinusitis

Front 34

How is PPID diagnosed?

Back 34

clinical signs
CBC: mature neutrophilia, lymphopenia
Chem: hyperglycemia
inc. serum insulin
inc. resting serum ACTH
neg. dex suppression test: gold standard

Front 35

How is PPID treated?

Back 35

management/ husbandry: good nutrition, regular deworming, dental care, vaccs & hoof care, keep coat clipped

pergolide: dopamine agonist (used most commonly)

cyproheptadine: serotonin antagonist