24 – Parathyroid Gland Flashcards

(27 cards)

1
Q

What is total serum calcium composed of?

A
  • Free (‘ionized’) calcium: 50%
  • Protein bound calcium: 40%
  • Complexed calcium: 10%
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2
Q

What are the main organs involved in calcium homeostasis?

A
  • Intestines: absorbed in the ileum (mediated by Vit D/calcitriol: except in horses)
  • Bone: stored and released (Ca release by action of PTH; inhibited by calcitonin)
  • Kidneys: excreted (PTH and Vit promote Ca reabsorption)
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3
Q

What mediates phosphate homeostasis?

A
  • Released from bone (stimulated by PTH)
  • Absorbed in small intestine (enhanced by Vit D)
  • *excreted in urine (increased by PTH); remainder in feces
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4
Q

Adult ruminants and phosphate homeostasis?

A
  • P mostly excreted in saliva (NOT urine); remainder in feces
  • Lactation and fetal development may be significant source of phosphate loss
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5
Q

Phosphate and transcellular shifting

A
  • P moves INTO cells with insulin and alkalemia
  • P moves OUT of cells with acidemia (secretory metabolic acidosis
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6
Q

What happens with parathyroid hormone abnormalities?

A
  • Ca and P tend to move in opposite directions
  • Ex. primary hypoparathyroidism
    o Decreased Ca
    o Increased P
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7
Q

What happens with Vit D abnormalities?

A
  • Ca and P tend to move in same direction
  • Excess Vit D
    o Increased Ca and P
  • Vit D deficiency
    o Decreased Ca and P
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8
Q

When might you see hypocalcaemia?

A
  • HYPOALBUMINEMIA
    o Decreased bound Ca?
  • Primary hypoparathyroidism
  • Nutritional secondary hyperparathyroidism
  • Hypovitaminosis D
  • Chronic renal failure (cats, most dogs, cattle)
  • Malabsorption with PLE
  • Anorexia in cattle
  • Ethylene glycol toxicity
  • Pregnancy, parturient or lactational hypocalcaemia/eclampsia
  • Acute pancreatitis
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9
Q

When might you see hypercalcemia? (HOGSINYARD)

A
  • Hyperproteinemia
  • Hyperparathyroidism
  • Osteolysis
  • Granulomatous disease
  • Spurious (lab or sampling error)
  • *IDIOPATHIC (cats) or iatrogenic
    • NEOPLASIA: apocrine gland ACA, LSA
  • Youth (puppy <6mo old)
  • Addison’s (hypoadrenocorticism)
  • Renal disease (horse, young dogs)
  • Excess (hypervitaminosis D)
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10
Q

What are the clinical signs with hypercalcemia? And values?

A
  • PU/PD, lethargy, inappetence, weakness
  • See with tCa >3.5mmol/L or iCa >1.6mmol/L
  • Life threatening with tCa >4.5mmol/L or iCa >2.2mmol/L
  • ***Metastatic calcification when product of Ca x P exceeds 6
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11
Q

What are the clinical signs with hypocalcaemia? And values?

A
  • Muscle tremors and fasciculations, facial rubbing, muscle cramping, stiff gait, seizures
  • See with tCa < 1.6mmol/L or iCa <0.8mmol/L
  • Cattle: recumbency with tCa <1.5mmol/L and life-threatening with tCa < 0.9 mmol/L
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12
Q

Humoral hypercalcemia of malignancy

A
  • Accounts for hypercalcemia in >50% of canine cases
  • Paraneoplastic syndrome usually due to secretion of PTH related protein (PTHrp)
    o Stimulates the same receptors as PTH
    o Increased iCa, low or low-normal P, decreased PTH, increased PTHrp
  • Occasionally due to tumor secretion of Vit D or osteoclastogenic cytokines
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13
Q

What are the most common tumours? (humoral hypercalcemia of malignancy)

A
  • Lymphoid neoplasms of T-cell origin
  • Apocrine gland adenocarcinoma of the anal sac
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14
Q

Idiopathic hypercalcemia in cats

A
  • Young to middle aged, DLH over-represented
  • (free) hypercalcemia w/o known underlying cause
  • Initially asymptomatic (months to years) but may progress
    o Weight loss, anorexia, vomiting, constipation, PU/PD
    o Calciuresis may lead to calcium oxalate urolithiasis
  • *diagnosis of exclusion
  • Treatment: diet, bisphosphonates (if symptomatic)
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15
Q

Idiopathic hypocalcaemia in cats: diagnosis of exclusion

A
  • Hypercalcemia is mild to moderate (iCa 1.4-1.9 mmol/L, total Ca <3.75mmol/L)
  • Serum P normal, PTH low or low-normal, PTHrp negative, 25-VitD is normal
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16
Q

Ca and CKD in cats/dogs

A
  • Most have normal serum Ca
  • Hypocalcaemia may occasionally be seen
  • Hypercalcemia is uncommon and tends to be mild
17
Q

What is hypocalcemia in some small animals with CKD driven by?

A
  • Progressive hyperphosphatemia
  • Leads to defective VitD metabolism by inhibiting renal 1alpha-hydroxylase
    o Decreased calcitriol
    o Decreased renal/intestinal Ca absorption
  • Activates FGF-23 (due to high P?)
    o Suppression of both calcitrol/PTH (initially)
  • High P complexes with Ca forming crystals that deposit in tissues
18
Q

What might hypocalcemia in some small animals with CKD lead to?

A
  • Renal secondary hyperparathyroidism
  • Low Ca, high P cause progressive increase in PTH synthesis
  • High PTH increases bone resorption and may lead to fibrous osteodystrophy (CKD-mineralized bond disease (MBD))
  • P also released from bone and hyperphosphatemia worsens
  • Progressive soft tissue mineralization
19
Q

Hypercalcemia is uncommon in some small animals with CKD?

A
  • Often reflects increase in ‘complexed’ fraction (these increase in renal failure)
    o Ca binds to citrates/phosphates
  • True hypercalcemia (increased free Ca) may reflect reduced renal clearance
20
Q

Concurrent hypercalcemia and CKD: which came first?

A
  • CKD may result in hypercalcemia, but hypercalcemia may lead to renal failure via mineralization of renal tissue
  • Cats/dogs: hyperCa more likely to be the cause of renal failure rather than the result of renal failure
    o SO investigate other causes of hypercalcemia first
  • Horses: more likely to have hyperCa b/c of CKD
21
Q

Horses lack renal 1alpha-hydroxylase (usually: converts Vit D to active form=calcitriol)

A
  • Likely due to high dietary content of Ca
  • Do NOT rely on Vit D for intestinal Ca absorption
    o Can develop hypocalcaemia with intestinal disease
22
Q

What is the major mechanism of elimination of dietary calcium in horses?

A
  • Renal excretion
  • Chronic renal disease often leads to hypercalcemia
  • Often accompanied by hypophosphatemia
23
Q

What is the approach to abnormal serum total calcium?

A
  • Rule out hyper/hypoproteinemia
  • Rule out age and obvious explanations
  • Recheck Ca to determine if persistent finding
  • Measurement of free calcium (blood gas)
  • Measurement of PTH (panel with iCa, PTH +/- PTHrp)
24
Q

How can you rule out hyper/hypoproteinemia?

A
  • Decreased/increased protein binding typically only causes MILD changes in total Ca
25
If a patient has hypercalcemia what should you do?
- Assess patient for neoplastic disease - Ex. check anal glands, lymph nodes, imaging studies
26
Nutritional secondary hyperparathyroidism
- Uncommon, but can occur in all species - Imbalance of Ca and P in diet o P:Ca > 3:1 or diet high in oxalates o Ex. grain diets in horses OR high organ meat diet in carnivores - Low free iCa stimulates PTH o Causes release of Ca from bone stores (osteolysis/osteopenia) o Lameness, bone pain, “big head” (fibrous osteodystrophy), pathological fractures
27
What are the common lab abnormalities with nutritional secondary hyperparathyroidism?
- Ca/P may be normal (or see mild decrease Ca and increase P) - +/- increased ALP (bone isoform) - Elevated PTH