Equine Parathyroid and Thyroid Disorders Flashcards
(16 cards)
describe calcium metabolism in horses
- very dependent on dietary intake
- excrete a LOT of calcium in the urine
- hypocalcemia: very common
- hypercalcemia: much less common
describe hypocalcemia causes in horses
- most common causes:
-colitis/GI loss!!!
-anorexia
-sepsis/endotoxemia - other causes:
-lactation
-transport
-exercise
-cantharadin toxicosis (causes colitis and GI loss with very low calcium levels)
-hypoparathyroidism: rare, idiopathic, usually critically ill foals
-nutritional hyperparathyroidism: rare
describe clinical signs of hypocalcemia in horses
- tachycardia, anxiety, muscle fasciculations, spasticity
- sometimes depression, ataxia
- thumps: synchronous diaphragmatic flutter
-phrenic nerve dysfunction = diaphragmatic contractions
-if you see, GIVE AND/OR CHECK CALCIUM - can progress to recumbency, seizures, and flaccid paralysis (end up like down cows, but down cows get so hypocalcemic so quickly that they skip this stage)
describe diagnosis and treatment of hypocalcemia in horses
diagnosis:
1. history and clinical signs
2. measurement of total and/or ionized calcium
3. evaluation for predisposing conditions
treatment:
1. IV 23% calcium gluconate
-rule of thumb: 250-500ml/horse/day
-amount to supplement depends on deficit severity
-admin SLOWLY and DILUTE or bradycardia!
- treat the underlying disease
- GET THEM TO EAT
describe hypercalcemia in horses
- much less common than hypocalcemia!
- most common cause:
-renal disease!
–increased calcium with renal disease is UNIQUE to horses (other animals become hypocalcemic)
–horses excrete a ton of calcium in the urine, so if the kidneys fail, calcium builds up - other causes:
-hyperparathyroidism: primary
-hypervitaminosis D
-hypercalcemia of malignancy - diagnosis:
-check phosphorous, calcium, PTH, PTHrP, and vitamin D levels
describe primary hyperparathyroidism
- primary: excess secretion of PTH due to tumor
- pathogenesis:
-increased renal and GI calcium absorption
-increased renal phosphorous excretion
-increased bone resorption
-results in increased calcium, decreased phosphorous, and increased PTH - RARE in horses
describe secondary hyperparathyroidism
- excess secretion of PTH in response to chronic HYPOcalcemia and/or HYPERphosphatemia
- 2 mechanisms:
-renal: usually, increased phosphorous and decreased calcium with renal failure results in increased PTH (but horses are opposite in renal disease so this is really rare in horses!!)
-nutritional: does occur but uncommon now with current equine diets
describe nutritional secondary hyperparathyroidism
- also called bran disease or big head disease
- causes:
-diets high in phosphorous and/or low in calcium (P:Ca >3.1) causes increased PTH and therefor bone resorption
-OR diets high in oxalates (that inhibit calcium absorption), like toxic plants - signs:
-facial enlargement: accumulation of unmineralized connective tissue in face/head that replaces bone
-dental issues: resorption of bone around tooth roots
-lameness, stiff gait: osteopenia, fractures - diagnosis:
-elevated phosphorous + normal or low calcium and elevated PTH - can recover with appropriate diet, rest, and TIME (9-12 months)
describe hypervitaminosis D
- many plants contain vitamin D-like compounds
-solanum spp, cestrum diurnum - mechanism:
-increased dietary vitamin D causes increased GI and renal absorption of calcium and phosphorous causes decreased PTH
-results in parathyroid atrophy
-mineral deposition in kidneys, muscle, ligaments, tendons, heart, etc. - signs:
-lameness
-stiffness
-reluctance to move
-depression
-weight loss
-heart issues - diagnosis:
-elevated phosphorous, usually elevated calcium, decreased PTH, elevated vitamin D - treatment:
-remove toxic plants and feed diet low in calcium and phosphorous
- +/- steroids to inhibit GI calcium reabsorption and cause calciuresis
-often unrewarding and prognosis usually poor because is hard to unmineralize tissues
describe hyeprcalcemia of malignancy
- paraneoplastic syndrome
-usually seen in lymphoma in horses - mechanism:
-tumor secretes PTHrP, a PTH agonist, which increases calcium resorption and phosphorous excretion - diagnosis: low phosphorous, increased calcium (usually), low PTH, high PTHrP
- treatment: remove cancer
- prognosis: poor
describe magnesium
- vital cofactor for important enzymatic reactions
-important in excitable tissues (nerve, muscle): membrane stabilization, nerve conduction, ion transport, physiological calcium blocker
-total versus ionized
-necessary for PTH activation - hypermagnesemia is rare in all species
-usually iatrogenic
-inhibits nerve and muscle function, leading to paralysis and collapse
-CAN BE FATAL (Mg overdose can be a method of euthanasia following anesthesia, can also be fatal if give too fast!! DILUTE AND GIVE SLOW)
describe hypomagnesemia in large animals
- general signs
-tachycardia, agitation, fasciculations, tetany
-arrhythmias, seizures, death - may see Mg disorders alone or with other electrolyte disorders
-hypocalcemia
-hypokalemia
-often cannot correct other electrolyte disorders until magnesium is corrected
-CMPK is magic - in horses:
-see with colitis, sepsis, cantharidin, anorexia
-CHECK and supplement if needed!! - in ruminants (cattle):
-also called grass tetany
-cool season grasses (spring and fall) are often low in Mg
-lactating animals on deficient pastures, leading to chronic hypoMg
-stress (cold weather, transport) usually precipitates signs
-signs: hyperexcitable, ear twitching, muscle fasciculations, bellowing, galloping, staggering, ataxia, recumbency, seizures, death
describe regulation of thyroid levels
- too much thyroid hormone = hyperthyroidism
-high metabolism leads to weight loss usually despite excellent appetite
-agitation
-unkempt greasy hair coat
-tachycardia
+/- GI signs: vomiting - too little = hypoparathyroidism
-low metabolism leads to weight gain
-cold intolerance/hypothermia
-exercise intolerance/lethargy
-alopecia
- +/- bradycardia
describe benign thyroid adenoma
- COMMON in older horses
- uni or bilaterally enlarged
- NOT FUNCTIONAL so TH levels are normal
- diagnosis: PE + age +/- ultrasound
- treatment: benign neglect unless:
-signs related to hyper or hypothyroidism
-HUGE mass = dysphagia, dyspnea, ulceration
-surgical excision is possible but risky
describe hyperthyroidism in horses
- reported but RARE
- functional thyroid carcinoma
- clinical signs: weight loss, behavior changes, HUNGRY, tachycardia
- diagnosis: ultrasound and increased TH
-AND make sure they are not on kelp supplement (contains lots of iodine) - treatment:
-surgical excision: same risks as adenoma
-medical Rx:
–options for SA are HELLA expensive for horses
–propylthiouracil: interferes with TH synthesis at multiple levels
describe hypothyroidism in horses
- frequently “diagnosed” in horses with obesity, insulin dysregulation, and laminitis
- experimental hypothyroidism in horses:
-cold intolerance, hypothermia
-bradycardia
-lethargy
-decreased appetite
-exercise intolerance
-NOT obesity insulin dysregulation, or laminitis - true hypothyroidism is VERY rare
-neonatal foals with congenital thyroid issues
-sudden discontinuation of TH supplementation - low TH levels are common but do NOT equal hypothyroidism
-may see age/breed specific normals
-thyroid axis suppressed in illness/stress: malnutrition, transport, systemic disease, resulting in non-thyroidal illness syndrome or sick euthyroid
-drugs and supplements - accurate diagnosis REQUIRES:
-stimulation testing: give TRH and measure TH
-measurement of TSH (not available in horses, yay)