Endocrine Flashcards
Cycle leading to clinical disease w/ insulin dysregulation
Feed abundance –> Increased adipose stores –> temporary adverse effects of adipose stores –> continued feed abundance –> temporary effects become permanent –> clinical disease
Pathophys of EMS revolves around (2)
- increased adipose stores
2. Insulin dysregulation (ID)
what is insulin dysregulation?
- excessive insulin response to NSC
- fasting hyperinsulinaemia
- insulin resistance - which is a normal response by cells to a normal level of insulin – to achieve a normal response by cells insulin levels increase
how does obesity affect ID?
- inflammatory cytokines produced by fat
- adipokines produced by fat
- excessive metabolism of fat in cells = lipotoxicity
—> interferes w/ insulin signalling, causing insulin resistance/dysregulation
how are obesity, insulin and laminitis linked?
- adipose - increases circulating inflammatory products
- increased insulin shown to cause laminitis + increased glucose may affect laminar vessels
predisposing factors to laminitis?
- excessive pasture exposure
- carbohydrate overload
- endotoxaemia, systemic sepsis or toxaemia
- supporting limb laminitis-laminar failure
- equine metabolic syndrome/PPID
- previous episodes of laminitis
- corticosteroids w/ concurrent metabolic disease
clinical signs of laminitis
- acute onset of lameness (bilateral)
- forelimbs > HLs
- reluctant to bear weight, land heel first - ‘heel-toe’ gait
- look uncomfortable behind
- increased digital pulses
- more sore on hard ground, worse on the turn
laminitis hoof tester pain location
front of frog
foot exam - laminitis findings
- palpable depression at the coronary band if there is sinking
- penetration of sole: discolouration, softening, draining pt w/ severe rotation
- hoof tester pain in front of frog
laminitis blocks to
abaxial nerve block
acute laminitis management
- tx primary disease and remove predisposing factors
- confinement
- sole support-palmar half of foot to point of frog: sand box, sole pack, dense foam, support shoes
- analgesia + NSAIDs: flunixin/bute
post acute laminitis management
- farrier: rocker toe (bring break-over back), bar shoe w/ sole-pack/palmar support
- reg hoof care + analgesia
- rpt rads to monitor progression
- avoid predisposing factors
EMS CS
- breeds (ponys), 6-20yo
- obese, regional adiposity
- laminitis
EMS ddx
PPID, hypoT?
EMS dx
- in feed glucose test/oral sugar test
- mod. insulin tolerance test
fasting insulin levels consistent w/ ID
> 20-30uU/ml
describe oral sugar test to dx EMS
- fast as baseline insulin
- 15ml/100kg corn syrup
- blood at 60 + 90 mins, normal insulin <45 and 60uU/ml
describe in-feed glucose test to dx EMS
- overnight fast
- give 0.5-1g/kg BWT glucose powder in non-glycaemic feed
- measure serum insulin and plasma glucose after 2hrs
- normal:
0.5g/kg 2hrs <60uU/ml
1g/kg dose 2hr insulin <90uU/ml
goal of EMS management
decrease ID and restore insulin sensitivity
–> weight reduction: exercise, decrease intake, decrease NSC
EMS diet management
- consume 1.5-1% body weight
- limit grazing 1hr TID vs. muzzle (only late night/early morning graze)
- less than 10% NSC - remove grain/concentrates/treats
- no pasture access during growing season
- soak hay
diets to maintain energy intake BUT w/ a low glucose and insulin response to manage non-obese EMS
- soaked beet pulp
- soaked soy hulls
- rice brain
- no fat supp
drugs to use for EMS
- thyroxine
- metformin
MOA metformin in EMS
- decreases glucose uptake, utilisation and systemic absorption
- cause a signif. decrease in plasma glucose and insulin
PPID signalment
> 15 yo, fluffy (hypertrichiosis), cushings
pathophys of PPID
- primarily hypothal disease
- loss of dopaminergic inhibition of the pars intermedia
- leading to hyperplasia or adenoma formation of the pars intermedia
- oxidative stress and increased genetic risk
what causes clinical disease in PPID
CS dt increased circulation of POMCs and loss of neuroendocrine function of adjacent tissues
CS of PPID
- hypertrichiosis - late CS
- LAMINITIS (POMC –> ID)
- hyperhydrosis
- supraorbital fat pads/bags under eyes
- weight loss/wasted topline + pot belly
- PU/PD
- lethargy
- recurrent infections (dt suppression of IL-1, T-cells, APCs)
less common CS of PPID
- Neuro: blindness, collapse, seizures
- infertility?? age related
Clinicopath abnormalities of PPID
- mild anaemia
- leukocytosis
- hyperglycaemia and glucosuria
- hyperinsulinaemia
- cortisol not indicative
+/- hepatic enzymes
dx of PPID
- ACTH stims –> measure increased POMCs
- TRH stim test –> testing hypothal pit axis
- Dexamethasone suppression test –> tests hypothalmic pituitary adrenal axis
ACTH stim test as dx of PPID
- reference ranges vary depending on time of year and geographic location
- horses that exceed the reference interval do not necessarily have the disease - needs to be taken in light of CS
- ‘grey zone’ –> rest test during best time OR TRH stim
- best time to test: FEB- APRIL (peak of dynamic phase)
management of PPID horse
- reg. teeth care + worming
- aggressive tx of infections
- address laminitis/risk + hoof care
- pharmacological: pergolide
pergolide MOA in PPID horse
Dopamine agonist –> increases dopaminergic control of the pituitary gland using dopamine agonists
response to pergolide tx in PPID horses monitoring
7 days: ACTH levels improve
30 days: improved demeanour/attitude, ACTH/other hormones
6 months: hair coat improvement
Long-term: other CS improvements
recommended protocol for PPID/ID horses
- Document findings:
- baseline feet
- plasma ACTH
- insulin concentration/in-feed glucose test - Encourage O to monitor appetite, hair coat, water intake, urination, BCS and general demeanour monthly
- Pergolide low dose –> reassess in 1-2months
- One or more CS should have improved + ACTH improved
* ** test at same time of day and under the same conditions
4b) if no improvement –> increased pergolide by 0.001mg/kg —> until max dose 0.01mg/kg reached
5. Vet monitor 2x/yr ongoing
describe the progression of CS with hyperlipidaemia
- Initial: assoc. w/ primary disease
- depression, failure to drink, lethargy, reduce GIT motility and faecal output - Mid: mild colic (stretching liver capsule), D+, icterus, SC oedema, CNS signs, HE
- Late: recumbency, convulsions, death
Clinical course: days to 3 weeks
dx of hyperlipidaemia
TGL >85mg/dl up to 500mg/dl
dx of hyperlipaemia
TGL >500mg/dl and opalescent plasma
other clinicopath parameters of hyperlipaemia
- liver enzymes elevated
- azotaemia
- glucose
- metabolic acidosis
treatment goals of hyperlipaemia
- Tx primary disease
- Improve energy intake and balance: IV glucose
- Decrease circulating TGL and improve uptake by peripheral tissue
- Tx liver disease
hyperlipaemia prognosis and mortality
- Primary: mortality 80%
2. Secondary mortality 25-50% (depends on underlying dz)
re. calcium homeostasis horses have —
- high total and ionized calcium concentrations
- poorly regulated intestinal calcium absorption
- high urinary fractional excretion of calcium
- low serum concentration of Vit.D metabolites
acute CS of hypocalcaemia
- when calcium is low sodium channels become activated by smaller changes in the RMP causing CS of increased neuromuscular excitability
- decreased extracellular calcium leads to decreased smooth muscle contractility
- –> tremors
- –> SDF: synchronous diaphragmatic flutter (frenic nerve stim. of diaphragm)
CS of lactation tetany
- can occur from 2wks prior to foaling up to weaning dt large loss of calcium in milk
- varied CS: profuse sweating, termors, anxious expression, tachy +/- arrhythmia, ileus, may present w/ colic
tx of SDF
- self correct once alkalosis resolved + lytes replaced orally via feed/water
- or IV calcium
how do you give calcium borogluconate?
500mls Ca borogluconate in 5L until CS improve then slow to 50mls/hr
what conc. of calcigol is safe at 3x maintenance?
20ml/L
divisions of hypercalcaemia by cause
- Dt parathyroid dysfunction–> primary vs. secondary
2. Independent of parathyroid dysfunction
what causes nutritional secondary hyperparathyroidism?
- diet rich in phosphorous and low in calcium
- high oxalate pastures
- -> increased PTH
CS of nutritional secondary hyperparathyroidism
- enlargement of the facial bones
- shifting lameness
- loose teeth
- pathologic fxs
dx of nutritional secondary hyperparathroidism
- Bloods: serum calcium normal/low, P normal/high, serum PTH increased
- Urinary fractional excretion of calcium is low + phosphorus high >4%
- Faeces: Ca:P ratio elevated dt oxalates
tx of nutritional secondary hyperparathyroidism
- Diet: Ca:P ration >4:1 (increase lucerne hay, reduce grain and supp. calcium)
Prevention diet: Ca:P ratio >1:1
influences of baseline thyroid levels
- age, daily rhythm, environment, exercise
- non-thyroidal illness syndrome
- decreased T3 and T4 dt corticosteroids, higher dietary iodine, PBZ
tx of hypothyroidism
- synthetic thyroxine
- iodinated casein
- bovine thyroid extract
what is anhidrosis?
- decreased ability to sweat in response to hyperthermia
dx of anhidrosis
intradermal sweat test w/ terbutaline dilutions
- normal horse sweats at 1:1,000,000
tx of anhidrosis
- move to cooler/drier climate + aircon boxes
- supplement thyroxine
- feeding combination of KCl and NaCl for chloride replacement
