Equine Lipid and Metabolic Disorders Flashcards
(21 cards)
describe hyperlipidemia/hyperlipemia in horses
- can occur in any horse but more often in:
-ponies, mini donkeys, morgan horses
-obese equids
-equids with metabolic syndrome or other endocrine diseases - increased metabolic demand helps development:
-pregnancy
-lactation
-concurrent illness - when in negative energy balance, start to mobilize fat for energy
- fat goes to liver and is:
-oxidized for TCA cycle for energy
-repackaged and released as VLDL (horses love to do this)
-resynthesized as TG and stored in liver (if all above are exhausted or unavailable)
describe clinical findings of hyperlipidemia/hyperlipemia
clin findings:
1. lethargy
2. dull mentation
3. decreased to absent appetite
4. other signs or primary disease
if hepatic lipidosis develops:
-mentation changes
-ataxia
-mild colic, diarrhea, fever
-sudden death can occur with hepatic rupture (rare)
describe diagnosis of hyperlipidemia in horses
- history and signalment
- body condition
- triglyceride concentration:
-normal <100mg/dL
-hyperlipidemia: 100-500mg/dL
-hyperlipemia: >500mg/dL with grossly lipemic (milky white) serum/plasma - if hepatic lipidosis develops:
-concurrent lab evidence of liver disease (increased liver enzymes) and/or insufficiency (increased bile acids or ammonia)
-fat ID on US (presumptive) or liver biopsy (definitive)
-if renal lipidosis develops: +/- azotemia
describe treatment of hepatic lipidemia/lipemia
GOAL: correct energy balance and stop lipid mobilization
- treat/manage underlying cause
- provide a source of glucose: IV dextrose, nutritional support (enteral: free choice or via intubation or parenteral)
- insulin: decreases lipolysis
- heparin: decreases lipolysis and promotes lipid uptake into adipose for storage
prognosis:
-fair without hepatic lipidosis
-guarded once hepatic lipodosis occurs (esp grave is progressed to hepatic insufficiency)
-prevent obesity!
-prevent/manage equine metabolic syndrome
describe equine metabolic syndrome
-a collection of metabolic and clinical features that include insulin dysregulation (ID) as a consistent component resulting in an increased risk of laminitis in horses and ponies
-additional metabolic or clinical features may be inconsistent
describe the 3 main components of insulin dysregulation
- basal hyperinsulinemia: increased insulin concentration at baseline or rest (without a meal)
- post-prandial hyperinsulinemia: increased insulin concentration following a meal
- tissue insulin resistance: more insulin is required to evoke the same response in the tissues (to take up the same amount of glucose, requires more insulin in a patient)
EMS can have 1, 2 or all 3 components as a feature of their disease
describe the pathophysiology of EMS
- poorly understood; potentially an adipose-derived endocrinopathy
-lots of different factors at play
-is NOT PPID or hypothyroidism - hyperinsulinemia leads to laminitis
-in normal horses and ponies, a high dose insulin infusion causes clinical signs of laminitis within 48 hours
describe the signalment and clinical signs of EMS
- age: adult to middle aged
- breeds:
-morgans, TWH, paso finos, saddlebreds, arabians, andalusians/lusitanos, warmbloods
-many pony breeds, mini horses, and donkeys - clin signs:
-generalized obesity: most often but not always
-regional adiposity: crest of neck, top of withers, behind shoulders. truncal, tail head
-laminitis: acute, chronic, or acute on chronic
-occasionally: mammary/preputial edema, pedunculated lipomas, infertility
describe diagnosis of EMS
- clinical signs:
-obesity and/or abnormal fat distribution (most often)
-laminitis - evidence of insulin dysregulation:
-static tests: baseline insulin concentration
-dynamic tests: oral sugar test, insulin tolerance test, combined glucose insulin tolerance test - laminitis:
-radiographs
-venograms
describe obtaining baseline insulin concentration for EMS diagnosis
process:
1. horse is fed hay but no grain
2. single blood sample collected for insulin (and often glucose, may also check leptin, adiponectin, and triglycerides)
advantages:
1. easily done in field
2. useful first step
3. high resting insulin indicates increased risk for laminitis
disadvantages:
1. static test, single time point
2, variation with diet, stress, exercise
3. less sensitive (only evaluates baseline hyperinsulinemia)
describe oral sugar test for diagnosing EMS
MOST COMMON test in the US
process:
1. fast 3-6 hours
2. collect sample for baseline insulin (and often glucose, leptin, adiponectin, triglycerides)
3. admin LIGHT karo syrup by mouth
4. collect samples at 60 and 90 min for insulin (and often glucose)
pros:
1. high insulin indicates increased risk of laminitis
2. evaluates both baseline AND post-prandial hyperinsulinemia
cons:
1. fasting
2. affected by stress, GI transit/absorption time
3. time waiting for sample collection
describe the insulin tolerance test for diagnosing EMS
process:
1. do NOT fast
2. collect blood sample for glucose at baseline (could also measure insulin here too, maybe leptin, adiponectin, triglycerides)
3. admin regular insulin IV
4. collect blood sample for glucose at 30 min
5. feed small amount of grain and hay, monitor glucose out to 60-75min
pros:
1. evaluates tissue insulin resistance
cons:
1. risk of hypoglycemia
2. affected by diet, stress, GI transit/absorption time
3. time waiting for sample collection
4. less informative of risk of laminitis!!!!
describe the combined glucose-insulin tolerance test for diagnosing EMS
process:
1. do NOT fast
2. collect blood sample for glucose at baseline (could also measure insulin here too, maybe leptin, adiponectin, triglycerides
3. admin glucose (oral or IV) and insulin (IV)
4. collect serial blood samples for glucose, insulin
pros:
1. evaluates tissue insulin resistance
2. often reserved for research
cons:
1. risk of hypoglycemia
2. time waiting for sample collection
3. less informative of risk of laminitis
describe adipokines and dyslipidemia
- leptin: increases with generalized and/or regional adiposity
-not always with insulin dysregulation (ID) or laminitis risk though - adiponectin: decreases associated with ID and an increased laminitis risk
- triglycerides: increases with generalized and/or regional adiposity, ID, and an increased laminitis risk, esp when in a negative energy balance
describe management goals for EMS
- manage insulin dysregulation
- reduce adipose tissue stores
- manage laminitis
via:
diet, exercise, medications, and monitoring
describe diet management for EMS
- all EMS horses need low glycemic index feedstuffs:
-non-structural CHOs (NCSs; starches and sugars) should be kept below 10-12%
-grass hay: ideally tested at <10%NSCs; if >10% or not tested, soak for 60 min to reduce NCSs
-no grain or low-NSC formulated grain only
-careful to provide protein/vitamins/minerals: ration balancers are a good option
-limited to no pasture or treats - overweight EMS horses: limit intake:
-start with 1/5% of body weight per day
-if resistant to weight loss, can decrease to 1.15% of body weight per day - lean EMS horses: allow maintenance/higher intake
-maintain with 2% BW per day
-gain with 2.5-3% BW per day
describe exercise management for EMS horses
- considerations:
-active laminitis limits exercise
-introduce gradually and monitor - improves body condition
- improves insulin sensitivity (even without change in body condition!)
describe medications for EMS management
- NOT a replacement for diet and exercise modifications
- levothyroxine:
-increases basal metabolic rate
-helpful in overweight cases resistant to weight loss
after 3-6 months or after weight loss is achieved, taper to 1/2 dose for 2 weeks, then to 1/4 dose for 2 weeks, then discontinue - metformin:
-poor bioavailability
-decreases enterocyte glucose absorption?
-helpful in cases with severe ID and signs (laminitis) while initial management changes are taking effect OR in cases with persistent ID despite optimal management
-rinse mouth and wipe lips after dosing to help avoid mucosal irritation with long-term use - SGLT2 inhibitors:
-flozins
-reduces glucose reabsorption in renal tubular allowing more excretion of glucose
-decreased glucose reabsorption and subsequent decreased insulin concentration
-helpful in cases with severe ID and signs (laminitis) OR in cases with persistent ID despite optimal managemet
-monitor for hypertriglyceridemia (usually without clinical signs) and other liver enzyme disruption
describe supplements for EMS management
- promising effects:
-spirulina platensis algae
-wheat bran protein aleurone
-polyphenol/amino acid blend with leucine - mixed effects:
-magnesium
-chromium
-short chain fructooligosaccharides - little benefit:
-cinnamon
-levocarnitine
-psyllium
describe laminitis management for EMS horses
- acute cases:
-sole support
-ice
-anti-inflammatories, analgesics - chronic:
-sole support: shoeing, trimming, time
-analgesics
describe monitoring and prognosis for EMS horses
- body condition:
-objective: scale, weight tape, body measurements
-subjective: assign BCS, describe regional deposits, photos - laminitis:
-digital pulses, heat over hoof wall, coronary band appearance, lameness (esp of hard surface in a tight circle) - repeat testing:
-at 3-6 months or once ideal BCS is achieved
-repeat OST
-measurement of insulin responses to current feeding practices - prognosis:
-EMS is more than just being overweight!
-risk of laminitis can be performance limiting and even limit quality of life
