Primary Hyperparathyroidism Flashcards
What’s the role of PTH, PTHrP, Vitamin D, and calcitonin in Ca2+ homeostasis?
- PTH is released in the face of low calcium to increase resorption from bone, absorption from intestines & kidneys (distal convoluted tubule, ascending loop of Henle), activates vitamin D, which increases Ca absorption from the intestines.
- PTHrP has similar actions as PTH, crucial in the fetus. In healthy adults, its virtually undetectable. Normal to low does not exclude the possibility of a neoplastic process, increased is usually associated with malignant cancer
- Calcitonin: role in limiting postprandial hypercalcemia. still a relatively minor role in calcium homeostasis
What’s primary hyperparathyroidism?
- uncommon in dogs, rare in cats
- high PTH despite high calcium levels
What are the causes of primary hyperparathyroidism?
- adenoma, carcinoma, or adenomatous hyperplasia
- metastasis
What’s the most common clinical complaint for primary hyperparathyroidism from owners?
signs related to urolithiasis or UTI
How does primary hyperparathyroidism cause PU/PD?
- calcium antagonizes the effects of vasopressin
- calcium inhibits tubular uptake of Na and Cl –> further inhibits urine concentration mechanism
How dose hypercalcemia lead to GI signs?
- decreased excitability and dysmotility of the intestines = decreased appetite, vomiting, and constipation
How does hypercalcemia lead to urolithiasis?
2 types of stones
- less resorption of calcium + increased excretion of phosphorus = calcium phosphate stone
- with increased calcium (oxalate) absorption from the GI, it can also lead to calcium oxalate stone formation
Which imaging modality is the most useful for investigating a dog suspected of having a PHPT?
ultrasound of the neck
90-95% patients with PHPT will have nodules (need experienced ultrasonographer)
What’s the mainstay therapy for pretreatment for hypercalcemia?
Fluid therapy. 0.9% NaCl 5-10ml/kg/h
can add in furosemide once patient is well hydrated
watch for hypokalemia
What are some other options to pre-treat the hypercalcemia?
- glucocorticoids (for hypercalcemia of malignancy)
- bisphosphonates
- calcitonin (salmon)
- plicamycin/ mithramycin
How many glands are usually enlarged for primary hyperparathyroidism vs. secondary?
1 vs multiple
What is the most successful definitive treatment options for primary hyperparathyroidism?
Surgery
What are some other options for definitive therapy for primary hyperparathyroidism?
- u/s guided ethanol ablation
- u/s guided heat ablation
What are some ECG changes in patients with hypercalcemia?
- ST segment elevation
- QT shortening
- arrhythmia
What’s the an emergency, short term treatment for hypocalcemia?
IV calcium gluconate
watch for long-term use - caustic to blood vessels
How frequent is feline primary hyperparathyroidism?
rare
What’s the treatment of choice for feline primary hyperparathyroidism?
surgery
What’s the long term prognosis post surgery for feline primary hyperparathyroidism?
good
What’s the prognosis for canine primary hyperparathyroidism?
short to mid-term (<2y) = excellent
long term is also good for all breeds, except Keeshond - recurrence = possible
What are the signs associated with hypercalcemia?
-Renal and Urinary Tract Signs
Polyuria
Polydipsia
Urinary incontinence
Stranguria
Pollakuria
Urolithiasis
-Gastrointestinal Signs
Vomiting*
Inappetence
Constipation
-Neuromuscular Signs
Depression
Exercise intolerance
Shivering*
Muscle twitching*
Seizures*
-Other
Dental pain
Difficulty eating
Stiff gait*
Lameness*
What are the signs associated with hypocalcemia?
- Signs Associated with Neuromuscular Excitability
Muscle fasciculations or tremors
Face rubbing, biting the paws
Hypersensitivity to external stimuli
Stiff, stilted gait
Tetanic seizures
Respiratory arrest - Behavioral Changes
Agitation
Anxiety
Vocalization
Aggression - Other
Panting
Hyperthermia
What are some post treatment considerations?
watch for hypocalcemia crisis
- muscle fasciculations, vocalizations, panting, tetany
What are some causes of hypophosphatemia?
- Decreased Intestinal Absorption
Decreased dietary intake
Malabsorption/steatorrhea
Vomiting/diarrhea
Phosphate-binding antacids
Vitamin D deficiency - Increased Urinary Excretion
Primary hyperparathyroidism
Diabetes mellitus ± ketoacidosis
Hyperadrenocorticism (naturally occurring/iatrogenic)
Fanconi syndrome (renal tubular defects)
Diuretic or bicarbonate administration
Hypothermia recovery
Hyperaldosteronism
Aggressive parenteral fluid administration
Hypercalcemia of malignancy (early stages)
-Transcellular Shifts
Insulin administration
Parenteral glucose administration
Hyperalimentation
Respiratory alkalosis
