Lecture 3 1/30/25 Flashcards
What are the clinical signs of hypercalcemia?
-PUPD
-acute kidney injury
-dehydration
-osteoporosis
-nausea
-vomiting
-constipation
-lethargy
-muscle weakness
-confusion/stupor/coma
What are the characteristics of a normal neuron?
-resting state of Na+ channels is stabilized by Ca2+
-Ca2+ prevents spontaneous depolarization
What happens to the neuron when there is hypercalcemia?
-Na+ channels are less likely to open
-neuron is harder to depolarize; threshold is increased
-neuron is less excitable
-patient exhibits slower/absent reflexes, slow muscle contraction, and confusion/stupor
What effect does hypercalcemia have on the heart?
can cause arrhythmia, such as bradycardia or AV block
What effect does hypercalcemia have on the brain?
can cause coma and/or seizures
What are the renal effects of hypercalcemia?
-nephrogenic diabetes insipidus
-PUPD
-calcium-oxalate crystals/stones
-AKI
What are the characteristics of acute kidney injury associated with hypercalcemia?
-renal vasoconstriction decreases GFR
-worsens with volume depletion
-reversible with volume expansion and lowering of serum Ca
How does the cause of hypercalcemia relate to the clinical manifestation?
-PHPTH: animal is not sick to minimally ill
-vitamin D toxicosis: animal is very sick
What is the diagnostic approach to hypercalcemia?
-confirm increase with iCa2+ measurement
-history
-physical exam w/ a rectal
-CBC/chem/UA
-PTH, PTHrp, and vit. D conc. measurements
-thoracic and abdominal imaging +/- neck ultrasound
-aspirate peripheral lymph nodes, liver/spleen, and bone marrow
What are the characteristics of hypercalcemia treatment?
-treat specific cause
-indications for treatment vary based on clinical signs and acute vs chronic onset
-specific treatment not needed if hypercalcemia is lab identified only and pet is not exhibiting clinical signs
Which clinical signs of hypercalcemia are severe and indicate need for immediate treatment?
-dehydration
-azotemia
-arrhythmia
-CNS signs/severe weakness
-tCa x phos > 60-80
What needs to be accounted for in the fluid plan for a hypercalcemic patient?
-dehydration %
-maintenance; increased if PUPD
-losses
What are the characteristics of fluid diuresis as an emergency treatment for hypercalcemia?
-use 0.9% saline at 2-3x maintenance
-may need to supplement K+
-increases Ca2+ excretion due to filtered Na+ competing with Ca2+ for renal tubular resorption
What are the characteristics of loop diuretics as an emergency treatment for hypercalcemia?
-maximize Na+ excretion, leading to calciuresis
-decreases renal Ca2+ reabsorption in thick ascending loop of henle
-patient must be hydrated first
What are the characteristics of glucocorticoids as a treatment for hypercalcemia?
-should not give before ruling out neoplasia; makes lymphoma diagnosis difficult due to lymphocyte lysis
-decreases Ca regardless of etiology
-decreases bone and intestinal absorption of Ca
-increases renal Ca excretion
What are the characteristics of biphosphonates?
-inhibit osteoclasts and prevent bone resorption
-used IV for emergency use in combination with other treatments
-can be given PO for maintenance in some diseases
What are the potential adverse effects of bisphosphonates?
-osteonecrosis of the jaw
-gastrointestinal upset
-esophagitis
What are the diseases that cause hypercalcemia?
-hyperparathyroidism
-osteolytic
-granulomatous
-spurious
-idiopathic
-neoplasia
-young animal
-addison’s
-renal
-D vitamin toxicosis
What are the mechanisms for hypercalcemia?
-increased PTH or PTH-rp
-increased calcitriol/vitamin D
-unknown
-non-pathologic
What are the different ways that increased PTH/PTH-rp and increased calcitriol/vitamin D can lead to hypercalcemia?
-increased absorption in the gut
-increased reabsorption in the kidneys
-increased resorption of bone
-decreased excretion in the kidneys
What are the characteristics of hyperparathyroidism?
-parathyroid-dependent mechanism of hypercalcemia
-can be primary
-can be secondary with renal or nutritional components
What are the characteristics of primary hyperparathyroidism?
-abnormal gland produces PTH
-chief cells function autonomously and do not respond to feedback from increased Ca
-can occur with solitary adenoma or hyperplasia
-normal glands atrophy
What is the result of excessive PTH due to primary hyperparathyroidism?
-increased Ca
-decreased P
How is primary hyperparathyroidism diagnosed?
PTH is inappropriately increased in the face of hypercalcemia; high-end normal or inc. PTH in the face of increased iCA
What is the signalment for primary hyperparathyroidism?
-uncommon in dogs
-typically occurs in middle to older age dogs
-keeshond dog breed has autosomal dominant PHPTH
-rare in cats
What are the clinical signs of PHPTH?
-possibly asymptomatic
-slow onset
-PUPD
-lower urinary tract signs
-weakness/hyporexia
What is the diagnostic workup for PHPTH?
-physical exam
-minimum database
-iCa and PTH/PTH-rp measurements
-neck ultrasound
-possible thoracic and abdominal radiographs
What is seen on a neck ultrasound in patients with PHPTH?
-one large, abnormal gland
-other normal glands atrophied
What is the treatment for PHPTH?
cervical exploratory surgery and parathyroidectomy; must leave 1 remaining gland to prevent hypoparathyroidism
What is important in post-op parathyroidectomy patients?
-monitor iCa
-supplement patients with calcitriol +/- calcium carbonate as needed until atrophied glands return to function
What is the prognosis of PHPTH?
-excellent prognosis following surgery
-poor prognosis if disease caused by malignancy or patient is in renal failure
-low recurrence rate in all breeds except Keeshond breed
What are alternative treatment options for PHPTH?
-ultrasound-guided ethanol or heat ablation
-medical management with PO bisphosphonates
What are the characteristics of secondary hyperparathyroidism?
-involves renal or nutritional abnormalities
-hypertrophy of all four parathyroid glands
What are the characteristics of renal secondary HPTH?
-driven by decreased calcitriol/vit. D in early stages
-driven by increased phosphorus in late stages
-can lead to renal disease progression
-can cause bone demineralization/fibrous osteodystrophy
-can lead to other non-specific, non-skeletal effects
What are the characteristics of calcium levels in renal disease?
-typically mild abnormalities
-tCa can be increased due to binding of inorganic ions or dehydration
-iCa can be increased, decreased, or normal
-iCa can change with changes in renal reabsorption/secretion or with decreased vit. D
What is nutritional secondary HPTH?
imbalanced diet with low calcium, low vitamin D, and/or high phosphorus leads to increased PTH secretion
What are the characteristics of neoplasia as a cause of hypercalcemia?
-most common cause of hypercalcemia in the adult dog
-third most common cause in cats
What are the neoplastic mechanisms of hypercalcemia?
-humoral hypercalcemia of malignancy/production of PTH-rp by tumor
-osteolysis
-other/ectopic production of PTH
Which cancer types can result in paraneoplastic hypercalcemia?
-apocrine gland anal sac adenocarcinoma
-lymphoma
-multiple myeloma
-carcinomas
How does neoplasia impact clin path measurements of calcium, phosphorus, and PTH?
-tCa increases
-iCa increases
-phos decreases or is low-normal
-PTH is 0 to low-normal
-PTH-rp is sometimes increased, sometimes normal
What is important about PTH-rp as a diagnostic tool?
-presence of PTH-rp indicates neoplasia
-PTH-rp reading of 0 does NOT rule out neoplasia; not all tumors produce it
