Equine Med- Endocrine

kelseyfmeyer's version from 2016-10-03 18:50

PPID: Pituitary Pars Intermedia Dysfunction

Question Answer
PPID is kinda like horse ___ (dz)cushings
what is the HPA axis, what is normal for it?Hypothalamus-pituitary-adrenal axis, normally hypothalamus signals to the pituitary with CRH (corticotropin releasing hormone) , and the the pituitary uses ACTH to tell the adrenal glands what to do. The adrenal glands release cortisol as a response....if there is just enough/too much cortical, the cortisol has negative inhibition on the hypothalamus to stop it from signaling the pituitary. There are ALSO normally dopaminergic neurons which go specifically from the hypothalamus to the melanotrophs of the pituitary, and they are the inhibitory function in terms of telling the pituitary to stop secreting ACTH.
what happens in PPID to the HPA axis?So the dopaminergic neurons which go from the hypothalamus to the melanocytes of the pituitary to inhibit the ACTH secretion of the pituitary somehow crap out, and that means there is no inhibition on the pituitary to stop secreting ACTH, ACTH goes way up, which means the adrenals are continually stimulated which means the cortisol levels go way up
Soooo if the PPID is actually from the dopaminergic nerves not working, why do we see all these tumors?Because lack of inhibition of the melanocytes leads to hypertrophy of them as they are already secreting.. and the hypertrophy causes the adenoma.
what is the common signalment of a PPID horse? (age? breeds?)Older horses (15+ years typical), Ponies, Morgans esp prone but any breed can be affected
what are some of the common presenting CSs with PPID horses?(1) hirsutism (curly hair, winter coats usually not curly so that's how you know it's not a winter coat. Also it's non-seasonal) (slow hair shedding) (2) PU/PD (ADH is all wonkey) (3) pendulous belly (remember high steroid= catabolic activity on proteins=weak ab muscles) (4) abnormal sweating patterns (5) and looking overweight (fat redistribution) (6) LAMINITIS (7) lethargy (8) immunosuppression (lots of steroids!) (9) abnormal estrus
PPID Diagnostics: what tests would you wanna do to try to dx this? (which is the BEST test? Which is the most sensitive and specific test?) (3 tests)BEST TEST: Baseline ACTH test. (take blood test. is it higher than you expect it to be? prolly PPID-- test samples touchy tho, be careful). SENSITIVE/SPECIFIC TEST: The TRH (thyrotropin releasing hormone) stim test. Basically get baseline ACTH, inject them with TRH, see if there is a ~90% inc in ACTH or cortisol above the baseline. LASTLY, you can try a low-dose dexamethasone suppression test Give them a inj of low dose dex, then basically wait overnight and measure cortisol....cortisol SHOULD be <1ug/dL
which PPID dx test should you NEVER do if you have a laminitic equine?DONT DO LOW DOSE DEX SUPPRESSION TEST-- should never ever give steroids with laminitis
what do you need to keep in mind when you are doing tests to try to dx PPID?horses have NORMAL FLUCTUATION in the ACTH/CORTISOL SEASONALLY!! So results might be hard to interpret from July to November (lol) (normal for ACTH to spike late summer/fall/early winter-- makes sense, thats when they get their winter coat)
what can you use to manage PPID?can give a daily dose of a dopamine agonist (like pergolide mesylate) which basically gives them the dopamine that they were needing to tell the melanocytes to be inhibited. The other option is giving them a serotonin antagonist (like cyproheptadine) because serotonin inhibits dopamine so this indirectly lets there be more dopamine..... + strict diet and exercise routine
what is pergolide mesylate?dopamine AGONIST which basically acts like the damaged dopaminergic nerves to inhibit the melanocytes of the pituitary
what is cyproheptadine?This is a serotonin ANTAGONIST which is useful because sero antagonizes dopa, so if you antag the antagonizer, it lets dopamine be more active (basically indirect way to add more dopamine to inhibit melanocytes in pituitary)
what is the prog of PPID?ALL depends on laminitis status!! Improvement in clinical signs with management and medications

EMS: Equine Metabolic Syndrome/ misc problems

Question Answer
What is interesting about the relationship between EMS and PPID?common to have both concurrently (lol)
so PPID as to Cushings as EMS as to....Type 2 diabetic
what is happening in NORMAL insulin metabolism?So as blood glucose in body goes up, stimulates the panc to release insulin. The insulin acts on adipose, skele mm, and liver and tells them to take up the glucose, which brings the blood glucose back down to normal
what is the problem with the insulin metabolism in EMS?Just like type 2 diabetes, the problem is that THE TISSUES DON'T RESPOND TO THE INSULIN, not that there isnt enough insulin. (insulin resistant tissues) (there are many mechanisms as to why they don't respond but said its not important that we know these)
so what is the main problem with EMS?BLOOD GLUCOSE IS TOO HIGH (bc tissues non-responsive to insulin so wont take it up)
explain why EMS might be a "vicious cycle" problemSo not sure which comes first, insulin resistance, hyperinsulinemia, or the genetics/obesity/PPID/systemic inflammation thing.
is EMS genetic?there def seems to be some horses that are more genetically prone but not sure of mechanism
explain how steroids relate with EMS, and what implications does this have for concurrent dzs?We know that if you give a horse a dose of steroids, that horse becomes transiently insulin resistant. So if they are PPID they always have high steroids (cortisol) in their system so they are kinda always insulin resistant (hence PPID and EMS often concurrent)
how does systemic inflammation relate to EMS?if they have inflammatory stuff going on, they are also transiently insulin resistant. (Which is why you might see high glucose in a strangulating lesion pt or sthing)
what is the main signalment of a EMS horse? (age? breeds?)Young to middle aged (if only EMS-- obv if older horse with PPID then it can be an older horse)....have always seemed to be an "easy keeper" (aka give them a flake of hay and they will get fat). Ponies, Morgans, Arabians, Paso finos are all more predisposed but anyone can get this.
what are the clinical signs/presentation like for EMS?These guys tend to typically be obese, and are prone to/have laminitis. You will see abnormal fatty deposits on them, and have a thick cresty neck. You will also see a big fat pad in that *supraorbital fossa near ear above the eyes... but aside from obesity and laminitis, dont really see the other PPID signs (weird haircoat, PU/PD, weird sweating patterns, etc)
what is nearly a pathognomonic sign of EMS?see a big fat pad/deposit in that *supraorbital fossa near ear above the eyes
explain why fat tissue isnt all the good for youExcess adipose tissue produces inflammatory cytokines!! such as TNFα & IL1 which can act both locally AND on the vascular endothelium-->THINK ABOUT THE LAMINAE/LAMINITIS! (its like having low grade inflammation at all times-- and think about the laminitis risk!!)
explain the factors EMS and PPID both contribute to make a laminitis nightmareEMS: as a result of the hyperinsulinemia and the abnormal metabolism that goes on in that cell, the laminae pull apart and you get Insulin mediated epidermal dysplasia. THEN with PPID, you also see a lot of VAScULAR changes (bc excess cortisol is not good for your vessels) and the VEssels respond with vasoconstriction. And due to catabolic effects of steroids, get Protein depletion= laminae pull apart. obv both dzs have risk for laminitis, and if you have BOTH dzs, you are at esp high risk.
horse with PPID is twice as likely to ____ as any other horsedevelop insulin resistance (bc steroids transiently cause insulin resistance)
*When do you NOT want to test for EMS in the horse?TESTS ARE NO GOOD WHEN THE HORSE IS STRESSED/IN A LAMINITIC EPISODE (stress= glucose release bc fight or flight etc)
so if you see a fat pony with laminitis and you first treat the acute laminitis and then you wanna see if its EMS or PPID, what two tests would you prolly do first?Baseline ACTH and a baseline Insulin and see if it tells you anything
how do you dx EMS? (3) (What is the most sensitive test for it?)BLOOD TESTS. and not the same ones as PPID. (1) Baseline glucose or insulin (kinda hard to interpret bc even if stressed from being poked in neck might cause inc of glucose) (2) MOST SENSITIVE TEST: Combined glucose insulin tests (basically give horse insulin and a CRI of glucose and see how they respond) (3) Neck Circumference Measurements-- bc they have fatty,cresty necks. So fat deposition in neck is a relatively sensitive way to look at this.
how do you want to manage the diet of a EMS horse?IF OBESE-- lose weight!! give Low sugar food, Limit grazing, exercise them
If there is concurrent PPID with the EMS horse, treat with...pergolide
what are the two medications you give to tx EMS?(1) Levothyroxine (2) Metformin
what is levothyroxine? why does it help with EMS?this is a thyroid hormone-- bc wanna inc their metabolism (and can inc insulin sensitivity for some reason)
what is metformin? why does it help with EMS?diabetes drug-- inc sensitivity of tissues to insulin
prog of EMS?Can lead a normal life with diet/exercise (but always dependant on laminitis status)
relation between PPID and insulin resistance?32% of horses with PPID are also IR, IR horses are twice as likely to PPID than normal horses
if the owner is like "MUH HURSE SICK BUT NO MONIES!??!!!" what can you do to try to tx both PPID and EMS before resorting to drugs?diet and exercise can help both
If you see this lumpy throated baby, what do you think is going on? goiter= thyroid hyperplasia- mom didnt get enough iodine when preggo
**what is the toxic plant which can mimic iodine deficiency in the diet?mustard plants
relationship between goiter and hypothyroidism?not all goiter=hypothyroid and vice versa
who tends to get hypothyroidism in horses?foals
hypothyroid/goiter foals are often born with what kinda clinical signs?Basically signs of pre/dysmaturity. Severe contracture of limbs, incomplete ossification of carpal and tarsal bones, prognathism (monkey mouth), or basically other issues with them not being mature enough to enter the world
how do you dz hypothyroidism in foals?hard to dx bc by the time they are born, hard to detect the hormone. Basically have to try to go off of CSs
is hypothyroid a death sentence for a baby foal?....depends on their CSs. if those carpal/tarsal bones aren't formed, thats a reason to put them to sleep.
how common is hypothyroid in ADULT horses?RARE!!!!! Yet a LOT of horses are “diagnosed” as such (Overuse of levothyroxine-- they prolly just have EMS and they are giving the levo and it works bc inc metabolism and inc sensitivity to insulin so tx EMS when they think they are treating hypoT)
Anhidrosis/Hypohidrosis: what is this?Basically they can't sweat! and this is the horse's main way to get rid of heat, so it's a big deal. It is a loss of β2 adrenergic control
clinical signs of Anhidrosis/Hypohidrosis?Exercise intolerant, high RR, no sweat, poor hair coat
how do you dx anhidrosis?Terbutaline test-- this is a Beta2 agonist. so you should just inject in skin and they should sweat where you injected it. If they don't, you got your answer
tx for anhidrosis?keep them cool!!
you see this pic of a horse..what are you thinking? BIG HEAD/ nutritional 2* hyperparathyroidism
what diet factors put horses at a risk to develop nutritional 2* hyperparathyroidism?diets where there is more P than Ca--- like bran!!
what are CSs of big head sz?(nutritional 2* hyperparathyroidism) bc not enough Ca in blood due to too much P binding it up, parathyroid kicks into high gear to pull Ca from the bone. Get osteolysis and abnormal bone lays down on top of it. usually facial bones affected first. main CS is they cant breathe bc bone is developing around nasal passages and cuts off airflow (need to do tracheotomy)
how do you treat big head?stop their weird diet. but the damage done is done. if they can breathe and organs (kidney) is functioning, can have a long happy life with enormous head.