Lecture 3 1/30/25 Flashcards

(41 cards)

1
Q

What are the clinical signs of hypercalcemia?

A

-PUPD
-acute kidney injury
-dehydration
-osteoporosis
-nausea
-vomiting
-constipation
-lethargy
-muscle weakness
-confusion/stupor/coma

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2
Q

What are the characteristics of a normal neuron?

A

-resting state of Na+ channels is stabilized by Ca2+
-Ca2+ prevents spontaneous depolarization

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3
Q

What happens to the neuron when there is hypercalcemia?

A

-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

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4
Q

What effect does hypercalcemia have on the heart?

A

can cause arrhythmia, such as bradycardia or AV block

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5
Q

What effect does hypercalcemia have on the brain?

A

can cause coma and/or seizures

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6
Q

What are the renal effects of hypercalcemia?

A

-nephrogenic diabetes insipidus
-PUPD
-calcium-oxalate crystals/stones
-AKI

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7
Q

What are the characteristics of acute kidney injury associated with hypercalcemia?

A

-renal vasoconstriction decreases GFR
-worsens with volume depletion
-reversible with volume expansion and lowering of serum Ca

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8
Q

How does the cause of hypercalcemia relate to the clinical manifestation?

A

-PHPTH: animal is not sick to minimally ill
-vitamin D toxicosis: animal is very sick

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9
Q

What is the diagnostic approach to hypercalcemia?

A

-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

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10
Q

What are the characteristics of hypercalcemia treatment?

A

-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

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11
Q

Which clinical signs of hypercalcemia are severe and indicate need for immediate treatment?

A

-dehydration
-azotemia
-arrhythmia
-CNS signs/severe weakness
-tCa x phos > 60-80

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12
Q

What needs to be accounted for in the fluid plan for a hypercalcemic patient?

A

-dehydration %
-maintenance; increased if PUPD
-losses

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13
Q

What are the characteristics of fluid diuresis as an emergency treatment for hypercalcemia?

A

-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

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14
Q

What are the characteristics of loop diuretics as an emergency treatment for hypercalcemia?

A

-maximize Na+ excretion, leading to calciuresis
-decreases renal Ca2+ reabsorption in thick ascending loop of henle
-patient must be hydrated first

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15
Q

What are the characteristics of glucocorticoids as a treatment for hypercalcemia?

A

-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

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16
Q

What are the characteristics of biphosphonates?

A

-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

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17
Q

What are the potential adverse effects of bisphosphonates?

A

-osteonecrosis of the jaw
-gastrointestinal upset
-esophagitis

18
Q

What are the diseases that cause hypercalcemia?

A

-hyperparathyroidism
-osteolytic
-granulomatous
-spurious
-idiopathic
-neoplasia
-young animal
-addison’s
-renal
-D vitamin toxicosis

19
Q

What are the mechanisms for hypercalcemia?

A

-increased PTH or PTH-rp
-increased calcitriol/vitamin D
-unknown
-non-pathologic

20
Q

What are the different ways that increased PTH/PTH-rp and increased calcitriol/vitamin D can lead to hypercalcemia?

A

-increased absorption in the gut
-increased reabsorption in the kidneys
-increased resorption of bone
-decreased excretion in the kidneys

21
Q

What are the characteristics of hyperparathyroidism?

A

-parathyroid-dependent mechanism of hypercalcemia
-can be primary
-can be secondary with renal or nutritional components

22
Q

What are the characteristics of primary hyperparathyroidism?

A

-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

23
Q

What is the result of excessive PTH due to primary hyperparathyroidism?

A

-increased Ca
-decreased P

24
Q

How is primary hyperparathyroidism diagnosed?

A

PTH is inappropriately increased in the face of hypercalcemia; high-end normal or inc. PTH in the face of increased iCA

25
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
26
What are the clinical signs of PHPTH?
-possibly asymptomatic -slow onset -PUPD -lower urinary tract signs -weakness/hyporexia
27
What is the diagnostic workup for PHPTH?
-physical exam -minimum database -iCa and PTH/PTH-rp measurements -neck ultrasound -possible thoracic and abdominal radiographs
28
What is seen on a neck ultrasound in patients with PHPTH?
-one large, abnormal gland -other normal glands atrophied
29
What is the treatment for PHPTH?
cervical exploratory surgery and parathyroidectomy; must leave 1 remaining gland to prevent hypoparathyroidism
30
What is important in post-op parathyroidectomy patients?
-monitor iCa -supplement patients with calcitriol +/- calcium carbonate as needed until atrophied glands return to function
31
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
32
What are alternative treatment options for PHPTH?
-ultrasound-guided ethanol or heat ablation -medical management with PO bisphosphonates
33
What are the characteristics of secondary hyperparathyroidism?
-involves renal or nutritional abnormalities -hypertrophy of all four parathyroid glands
34
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
35
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
36
What is nutritional secondary HPTH?
imbalanced diet with low calcium, low vitamin D, and/or high phosphorus leads to increased PTH secretion
37
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
38
What are the neoplastic mechanisms of hypercalcemia?
-humoral hypercalcemia of malignancy/production of PTH-rp by tumor -osteolysis -other/ectopic production of PTH
39
Which cancer types can result in paraneoplastic hypercalcemia?
-apocrine gland anal sac adenocarcinoma -lymphoma -multiple myeloma -carcinomas
40
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
41
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