Equine Endocrinopathies and Metabolic disorders Flashcards
PPID?
Pituitary Pars Intermedia Dysfunction
loss of dopaminergic inhibition of PI (due to neurodegeneration)
“Equine cushings”
High cortisol AND ACTH
What is the most common equine endo dz?
PPID
PPID incidence?
> 15 years
ponies and morgans
Pars intermedia is made up of ____ that produce ____ which is cleaved into _______.
melanotrope
POMC
alpha-MSh, beta-Endorphin
Pars distalis is made up of _____ that produce ___ and are cleaved into _____.
Corticotrophs
POMC
ACTH
Normal inhibitory control of melanotrophs?
Dopamine from hypothalamus
Positive control of melanotrophs?
TRH –> MSH (seasonal regulation)
PPID path landmarks
hypertrophy –> hyperplasia –> adenoma formation
PPID results in an abundance of ___.
ACTH, CLIP, beta-Endorphin, and alpha-MSH
PPID signs?
hirsutism - most common PU/PD Laminitis muscle wasting/weight loss bulging eyes XS sweating immunosuppresion infertility increased appetite lethargy/docile blindness, ataxia, seizures
Early signs of PPID?
delayed shedding
shift in metabolism
regional adiposity
+/- infertility problems
PPID dx?
Endogenous ACTH - check in morning , quick baseline test, affected by seasons (higher in the fall)
TRH stim - give TRH, measure blood ACTH (increase in ACTH and cortisol)
can also measure MSH in response to TRH
TRH stim test
need early morning blood sample and in fall
Dexamethasone suppression test
Give exogenous steroids, cortisol will not decrease, PI dx
antermortem gold standard
seasonal variations exist, need 2 farm visits
PPID treatment goals?
reduce clinical signs, avoid laminitis, dx and manage IR if present, may improve infertility
increase dopaminergic affect - dopamine agonists and serotonin antagonists
laminitis management
Pergolide
dopamine agonist (suppress PI activity) primary side effects are depression and anorexia
Permax/Prascend
PPID treatment $$$
cyproheptadine
serotonin antagonist
block ACTH production from PI
variable efficacy
Equine metabolic syndrome (EMS)
Insulin resistant
Obese/fat deposits
prior/current laminitis
“easy keeper” (low food requirement)
EMS incidences?
Ponies, morgans, paso fino, fjords
5-20 years old
most are obese
EMS clinical signs?
laminitis obesity easy keeper abnormal repro cycling cresty neck
Prolonged _____ can induce laminitis
hyperinsulinemia (>100)
EMS dx?
resting insulin/glucose concentration (>20-30)
oral sugar test if normal resting insulin - give light karo syrup, measure blood gluc in an hour, + if high glucose and insulin
combined glucose - insulin test
EMS treatment
improve insulin sensitivity by: reduce body fat avoid high starch/sugar feeds exercise (increase weight loss and insulin sensitivity) restrict pasture access no sugar cubes/treats Levothyroxine- ONLY SHORT TERM because hypothyroid meds but they help weight loss and and insulin sensitivity Metformin (PO pill)
Thyroid dysfunction
NOT like adult acquired hypothyroidism
Euthyroid Sick Syndrome or non-thyroidal illness syndrome - during sepsis
Primary site of Ca homeostasis?
GI
HypoCa conditions?
Synchronous diaphragmatic flutter (SDF)
lactation tetany
seizures
colic-endotoxemia
SDF
depolarization of phrenic nerve too fast, specific thumping sound horses anxious cln path: low Ca, metabolic alkalosis, Low K and Na Mg may also be decreased
Lactation tetany
pre-foaling to post-weaning
high sweat, anxious, tachycardia/arrhythnmia, colic
clin path: decreased Ionized Ca
treatment: IV Ca
Sepsis/Endotoxemia/Colic
common cause in hospital patients
G- bacteria –> LPS —> blood
horses especially senstive to endotoxemia
insufficient PTH secretion and INC Ca sequestration
Blister beetles
found in Alfalfa Cantharidin is toxic to all mucous membranes vesicant highly irritating colitis
Blister beetles toxicosis
fever, tachycardia/pnea, anorexia, colic, PD, dehydrated, hematuria
hypoCa leads to muscle fasciculations, sweating, arrhythmias and SDF
HyperCa incidence?
HypoCa» Hyperca
primary/secondary (nutritional) hyperPTH
hyperVitD
nutritional hyperPTH pathogenesis?
decreased Ca/XS P, oxalas
stimulates PTH
Ca and P mobilized from bone
bone —> fibrous connective tissue
secondary (nutritional) hyperPTH history and clinical signs?
low Ca, high PO4 diet
“big head”
bones of maxilla widen, loose teeth, shifting leg lameness
secondary (nutritional) hyperPTH dx?
nutritional history, clinical presentation
clin path: Ca low or normal, P normal or high, urinary fractional excretion (highP, lowCa)
secondary (nutritional) hyperPTH treatment?
increase Ca, decrease P in diet
change Ca:P ratio to 4:1 temporarily
normally 1:1-2:1
Anhidrosis
can’t sweat, commonly see splashing in water trough
Anhidrosis incidence?
SE US
no breed or sex predilection
Anhidrosis etiology?
Catecholamines –> sweat
etiology unknown! Acute –> chronic with irreversible gland unresponsiveness
Anhidrosis clinical signs?
gradual or acute onset
tachypnea at rest
hyperthermia
limited/failure to sweat during exercise
Anhidrosis chronic signs?
poor performance episodic fever spikes anorexia dry, flaky skin and/or alopecia decreased water consumption
Anhidrosis diagnosis?
only in research setting
terbutaline sweat test - won’t sweat with injection of terbutaline if anhydrotic
Anhidrosis treatment?
No evidence based treatment
remove from environment (AC) - can regain sweating ability
environmental management
