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What’s all this talk about…?. Equine Cushing’s Disease Insulin Resistance Equine Metabolic Syndrome. Dr. Meg deGravelles Tacoma Equine Hospital. Why care if my horse is…. Hairy Sway-backed Sweaty Poorly muscled Lethargic. Overweight An “Easy Keeper” Thirsty Funny shaped. Laminitis.

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What’s all this talk about…?


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    Presentation Transcript
    1. What’s all this talk about…? Equine Cushing’s Disease Insulin Resistance Equine Metabolic Syndrome Dr. Meg deGravellesTacoma Equine Hospital

    2. Why care if my horse is… Hairy Sway-backed Sweaty Poorly muscled Lethargic Overweight An “Easy Keeper” Thirsty Funny shaped

    3. Laminitis Horses with Cushing’s and Insulin Resistance are extremely prone to foundering

    4. Typical Cushing’s : -Older (>17 years old) -Ponies and Morgan horses are the most common breeds, but all breeds can be affected -No sex predilection -Long hair coat that doesn’t shed out properly -Sway-backed, pot-bellied, muscle loss -Inappropriate sweating -Lethargy -Abnormal fat deposition -Increased drinking, increased urination -Infertility -Increased susceptibility to infection -Chronic laminitis

    5. But what is Cushing’s? Also called Equine Pituitary Pars Intermedia Dysfunction (PPID) The “Quick & Dirty” definition: A disease most commonly caused by a benign tumor or overgrowth of the pituitary gland. The pituitary indirectly controls the body’s release of cortisol. Cortisol is a steroid that, when properly regulated, is critical to almost every body system. When the body can no longer “turn off” the flow of cortisol, systemic effects are seen, including the classic signs we recognize as being ‘Cushingoid.’

    6. What is Cushing’s? Recent evidence shows a more complex pathway: PPID is more likely a primary disease of the hypothalamus, which neighbors the pituitary. The hypothalamus has neurons that regulatedopamine release to the pituitary. Dopamine inhibits the pituitary’s release of “POMC” and related substances such as ACTH. Degeneration of these domaminergic neurons in the hypothalamus cause a loss of inhibition of the pituitary gland and, thus, excess production of ACTH. ACTH then causes the adrenal glands to release cortisol. Uncontrolled ACTH = uncontrolled cortisol = Cushing’s

    7. Whew! Take a breather! Okay, now back to work.

    8. Does my horse have Cushing’s? Unfortunately, diagnosing PPID can be a challenge. There are several tests, but none are foolproof. The best diagnostic indicator of PPID is the classic long, curly haircoat. So if you have the “Classic Cushingoid Pony,” why test? • GET BASELINE LEVELS to facilitate treatment, monitor progression of the disease, and make appropriate adjustments as his condition changes.

    9. Not all horses with Cushing’s have thisclassic long curly haircoat. For horses that are questionable, making a diagnosis is important- Early diagnosis and treatment may prevent the progression of clinical signs and the development of life-threatening disease or laminitis.

    10. What we recommend Physical exam Baseline CBC and Chemistry panels for other systemic issues The most appropriate Cushing’s diagnostic test for your horse    Concurrent insulin level check: Many horses with Cushing’s have concurrent insulin resistance (25-75%), and these horses are especially prone to laminitis. Therefore, we strongly suggest (and routinely run) a resting insulin level to use a prognostic indicator.

    11. Current Diagnostic Tests -Dexamethasone Suppression Test (DST) -Thyrotropin Releasing Hormone Stimulation Test (TRH) -Endogenous Plasma ACTH Concentration Test (ACTH) -Cortisol Rhythm Assay -ACTH Stimulation

    12. That doesn’t seem that complicated… What makes this hard: Seasonal variations: The pituitary gland is seasonally regulated, with greater hormone production in the fall (generally accepted as being late July through early November). This probably occurs as a natural process to prepare horses and ponies for harsh winter conditions. Unfortunately for us, this makes diagnosing Cushings far less accurate in the fall, as well as suspect in the spring transition. Lack of sensitivity/specificity: None of the available tests have been shown to be completely accurate, even in the ‘good’ time of year. Bottom Line: If a suspect horse comes back with negative results, we recommend re-testing in 4-6 months (but excluding the fall). OR we ‘treat empirically.’

    13. How do we treat PPID? 1. MANAGEMENT = SUCCESS 2. MEDICAL

    14. MANAGEMENT • Body Clipping 2. Correction of dental abnormalities & good dental maintenance 3. Regular and quality hoof care 4. Conscientious nutrition -Increased nutrition- amount & quality -Concurrent IR?-Supplements: Chromium Magnesium

    15. MEDICAL The previous mainstay of treatment was a seratonin antagonist called cyproheptadine. The current drug of choice is a dopamine agonist, Pergolide mesylate Pergolide is generally started at a low dose, and then is adjusted as the disease progresses or other issues emerge. In refractory cases (those that can’t be controlled with even the maximum dose of Pergolide), cyproheptadine can be added, though minimal research has been done on this.

    16. = SUCCESS

    17. Look familiar?

    18. Insulin Resistance

    19. What is insulin? Insulin is a hormone whose actions are widespread and profound on the body. Glucose is the food cells need to thrive and survive. Insulin’s main function is enabling glucose to enter into and ‘feed’ the cell. What is insulin resistance? Insulin resistance is simply a decrease in the body’s ability to respond to insulin. Therefore, to get glucose into the cell, more and more insulin is needed as cells become less sensitive to it.

    20. What causes insulin resistance? (“IR”) Some horses are at a higher risk for IR, due to several possible factors: 1.) genetic predisposition 2.) a diet high in sugar and starch 3.) inadequate activity and exercise4.) obesity and being overweight (BCS 7 and higher)5.) horses with Cushing’s

    21. 1. Genetic predisposition Morgans Arabians Pasos Ponies This is most likely related to their ability to survive and thrive on limited diets and in harsher environments. Note: all breeds can become insulin resistant.

    22. 2. Diet high in starch and sugars Here’s the (boring) “down-and-dirty”: -Starches and sugars are also called “non-structural carbohydrates”/NSCs. -Diets high in NSCs lead to high blood glucose. This leads to an increase in insulin. -This insulin causes glucose (much of it unneeded) to flood into the cell. -Once all this glucose is in the cell, the cell has no way to let it out. -What it can do, though, is make its membrane less sensitive to insulin. -Eventually, cells may lose their sensitivity to insulin to such an extent that the body can’t produce enough insulin to get glucose into the cells. -Then cells begin to starve, and muscle wasting results– but the abnormal fatty deposits remain.

    23. 3. Inadequate activity and exercise -Horses have evolved to be active and moving the majority of the day. -Our current management, along with the high levels of grain and good quality hays that horses in previous generations did not have access to, precipitate a decrease in insulin sensitivity. Note: While we’d all like to think “getting horses back in touch with nature” is a ideal, for some insulin resistance horses, this would be detrimental. It could be said that, for some horses, we’ve bred ourselves into stalls and dry lots.

    24. 4. Obesity and being overweight The current thought is that “Fat is an organ.” i.e. Adipose tissue itself produces more than 100 bioactive substances that affect many vital body functions, including regulation of inflammation and insulin sensitivity. Research is saying that increased fat = decreased insulin sensitivity. Note: While obesity is associated with IR, not all obese horses are IR, and not all IR horses are obese. It is simply considered a risk factor.

    25. 5. Horses with Cushing’s PPID causes high circulating levels of glucocorticoids. These steroids cause the body to lay down more adipose tissue (fat), which is directly related to a decrease in insulin sensitivity.

    26. Why do we care? LAMINITIS Current researchers believe IR makes horses susceptible to laminitis due to: -Laminar cells in the foot starved for glucose-Alterations in blood flow to the foot-As-of-yet undiscovered factors

    27. The typical IR horse: IR horses all generally share the following issues: Abnormal fatty depositsespecially @ the crest of the neck rump above the eyes Voracious appetite Excessive drinking & urinating Severe propensity for laminitis IR is often first noted between 4-12 yrs old, and often isn’t “acknowledged” & addressed until there is a laminitic episode. Remember: up to 25-75% Cushing’s horses are also insulin resistant. 

    28. Does my horse have IR? Diagnosing insulin resistance is fairly straightforward. • Given that most IR horses have high insulin levels in their blood, a single sample is taken and measured for this insulin concentration. Insulin over 30 uUnits/ml is considered hyperinsulinemic, and therefore diagnostic for IR. Rarely, this test is not sufficient, and another test can be performed: The combined glucose insulin test: multiple samples are taken and compared after giving the horse glucose.

    29. How do I treat? • Management: themainstay DIET! EXERCISE! Also, REGULAR & DILIGENT HOOF CARE is very important 2. Medical Thyro-L, aTHYROID HORMONE SUPPLEMENTis another helpful tool. 3. Minerals Supplementing CHROMIUM and MAGNESIUM is thought to help make the body more sensitive to insulin.

    30. So, whatta I do?? Feeding a horse with insulin resistance aka “Cruel to be kind” 1. CUT THE CARBS!! (aka “sugars,” “starches” “NSCs/non-structural carbohydrates”) -This includes forage as well as grains/pellets (‘concentrates’). -Overweight horses that are easy keepers can be placed on a diet of just hay and a vitamin/mineral supplement. It’s true!

    31. Cutting Carbs -Avoid all feeds with corn, oats, molasses, etc., which all have a very high sugar content. -There are currently some very good low NSC feeds on the market today if your horse’s weight can’t be maintained on hay alone, or if you need something to “disguise” your supplements. See the list we’ve provided for suggestions. -Restrain yourself in doling out treats, even apples and carrots. These too are sugar rich. -Underweight or working IR horses that need more calories than can be provided by hay can be fed a low NSC/low starch concentrate plus beet pulp if needed, which is a low-starch way to add calories.

    32. 2. Pasture Management Pasture grass is one of the largest sources of sugar in a horse’s diet !! -Any horse with IR should have restricted access to pasture, esp. at times of rapid pasture growth, such as the spring and fall. A good trick = when you start having to mow your lawn at home more, you should start holding your horse off of pasture. -Horses with a history of recurrent laminitic episodes should be restricted to dry-lot turnout. -With a wide spectrum in the severity of IR, consult the vet (us!) for our turn-out recommendations.

    33. Don’t forget-- Move that Boo-Tay!! aka: Get an exercise program going. Start slowly, and work your way up.

    34. Medical therapy So, you’re feeding your horse practically nothing and you’re riding regularly-- But he won’t lose a pound! Thyroid hormone supplementation: (Levothyroxine) Not a ‘silver bullet,’ but it can be a useful tool when diet & exercise alone hasn’t made enough change: • Calculate your horse’s appropriate weight. Use thyroid supplementation to “jump start” weight loss. Once your target weight is reached, levothyroxine is weaned off. • Can also be used long term to directly enhance insulin sensitivity in more severely affected horses. Note:While on thyroid supplement, horses must be off pasture and maintained on a strictly controlled diet – otherwise, they will PIG OUT!

    35. A grazing muzzle is a beautiful thing!

    36. It won’t be easy… But it CAN be done!

    37. What is…? EQUINE METABOLIC SYNDROME “EMS” is defined simply as the combination of obesity, insulin resistance, and concurrent laminitis. This is a very common, though unfortunate combination, because IR horses need lots of exercise, and laminitic horses need limited exercise. This makes dietary management and diligent hoof care even more important.

    38. A little picture to make us feel better: Even cavemen had fat horses!

    39. What’s fat? Many people use a system called the “Body Condition Score”(BCS #) It gives your horse a1-9 scorebased on fat (or lack thereof) at certainplaces, including the neck, withers, rump, tailhead, rib area, etc. Between 4-5 is considered ideal. Horses over BCS 7 are at risk for IR.

    40. Body Condition Score Here’s an example of a BCS 1-2   Here’s an example of a BCS 4-5 Here’s an example of a BCS 8-9  Note: a horse with a BCS or under 5 can still be IR, i.e. a horse can have ribs showing and still be insulin resistant.

    41. A little bit about… LAMINITIS

    42. What are the warning signs? Acute episode: Rocking back on hind end to take weight off of front feet Reluctance to walk Signs of pain & distress: SweatingHigh heart rateHigh respiratory rate Extremely strong‘digital pulse’ (digital artery along the back of the pastern) Note- ‘heat’ is not a reliable indication of pain or inflammation in the foot.

    43. Some other signs are less shocking,but suspicious for laminitis whether an acute episode or a flare up of a chronic problem: Shifting weight from one front foot to the other Rocking back on the hind end to walk, and especially to turn Bi-lateral tenderness to walk on rocks or firm surfaces when this has not previously been an issue A strong digital pulse in both front feet

    44. Chronic, low-level laminitis This is commonly seen in Cushing’s, IR, & EMS horses Horses that have previously foundered or have recurrent low-level episodes have less obvious signs. It is especially important to recognize these more subtle signs, becausethese horses are extremely sensitive to developing an acute and debilitating episode. - difficulty turning or pivoting on one foot - stiff or choppy gait in the front - changes in hoof shape and hoof growth

    45. CLUES in the foot: Stretched white line “Slipper Toe” Founder rings

    46. What should I do if I see these signs? CALL US! You already know the answer-- An episode of acute laminitis is an emergency! Early intervention can prevent or minimize irreparable damage.

    47. Once the acute episode has been diagnosed & stabilized (or a case of chronic founder identified) The next step is to enlist the help of aknowledgeable and experienced farrier. If you suspect your horse currently has low-level laminitis or has previously foundered: X-rays should be taken to diagnose and better manage your horse in the present, as well as in the unfortunate case of any future problem.

    48. One more note- Don’t Panic!! BEFORE AFTER BEFORE AFTER