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SA Medicine Endocrine > Parathyroid Disease > Flashcards

Parathyroid Disease Flashcards

1
Q

Where is 99% of calcium in the body?

A
  • 99% bone/teeth
  • Remaining 1% intracellular
  • 0.1% extracellular
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2
Q

Forms of calcium

A
  • 50-60% ionized (biologically active form)
  • 30-40% protein bound
  • 10% chelated/complexed (phosphate, citrate, sulfate, bicarbonate)
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3
Q

Where is parathyroid hormone made?

A
  • parathyroid glands
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4
Q

Where is calcitriol activated?

A
  • Activation occurs in the kidney
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5
Q

Where is calcitonin made?

A
  • Thyroid gland
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6
Q

What three hormones are involved in calcium regulation?

A
  • Calcitriol
  • Parathyroid hormone
  • Calcitonin
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7
Q

How many parathyroid glands are there?

A

2 pairs (4 total)

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8
Q

What cells in the parathyroid gland make parathyroid hormone?

A
  • Chief cells
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9
Q

Actions of PTH (broad)

A
  • maintain plasma ionized calcium levels

- Regulate plasma phosphorus levels

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10
Q

What three organs does PTH act on?

A
  1. Bone
  2. Kidney
  3. Small intestines
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11
Q

PTH effect on bone

A
  • Increase resorption (release) of calcium and phosphorus
  • Increases blood levels of both
  • Ultimately increases phosphorus and increases calcium
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12
Q

PTH effect on the kidney

A
  • Increase calcium reabsorption (distal tubules and collecting ducts)
  • Increase phosphorus excretion (proximal tubules)
  • Serum calcium goes up, phosphorus goes down
  • Also stimulates synthesis of the active form of Vitamin D (via increased activity of 1-alpha-hydroxylase)
  • Ultimately: Increases calcium and decreases phosphorus
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13
Q

PTH effect on small intestines

A
  • Indirectly via increase in calcitriol, leading to an increase in calcium and phosphorus
  • Ultimately: Increases calcium and increases phosphorus
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14
Q

What are the there places where calcitriol works in the body?

A
  1. Small intestine
  2. Bone
  3. Parathyroid glands
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15
Q

Calcitriol effect on the small intestine

A
  • Increases formation of calcium binding protein (CBP) which transports calcium from the lumen into the intestinal epithelial cells
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16
Q

Calcitriol effect on bone

A
  • In large quantities stimulates bone resorption thus increasing calcium and phosphorus
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17
Q

Calcitriol effect on parathyroid glands

A
  • Negative feedback leads to decreased PTH
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18
Q

Where is calcitonin made?

A
  • Parafollicular cells (C cells) of the thyroid
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19
Q

Function of calcitonin

A
  • Decrease serum calcium concentration
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20
Q

Calcitonin effects

A
  • Works on bone
  • Decreases osteocytic membrane activity
  • Decreases osteoclast formation
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21
Q

Significance of calcitonin compared to PTH

A
  • Much less significant
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22
Q

Look at the chart on Dr. Haines’s slides with the Ca/P summary - seriously do it! It’s helpful

A

do it

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23
Q

What happens to PTH as calcium goes up?

A
  • PTH will go down
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24
Q

What happens to PTH as calcium goes down?

A
  • PTH will go up
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25
Q

Calcium regulation general

A
  • maintained in a very tight range
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26
Q

What are the three components of total calcium?

A
  • Ionized, protein bound, and chelated forms
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27
Q

How would you confirm hypercalcemia if you have an animal with an elevated total calcium level?

A
  • Need to get an ionized calcium
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28
Q

Differentials for hypercalcemia

A

HOGS IN YARD

  • Hyperparathyroidism (1°)
  • Osteolytic
  • Granulomatous
  • Spurious
  • Idiopathic (cats), Iatrogenic (meds, supplements)
  • Neoplasia (lymphoma, anal sac adenocarcinoma)
  • Young
  • Addison’s
  • Renal disease
  • D toxicosis (vitamin D)
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29
Q

Which differentials for hypercalcemia are driven by PTH?

A
  • Hyperparathyroidism (primar)

- Neoplasia

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30
Q

Which differentials for hypercalcemia are not driven by PTH?

A
  • Granulomatous disease
  • Renal disease
  • Vitamin D toxicosis
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31
Q

What differentials for hypercalcemia are not driven by PTH and are also calcitriol driven?

A
  • Granulomatous disease

- Vitamin D toxicosis

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32
Q

Hyperparathyroidism mechanism of hypercalcemia

A
  • Increased PTH that does not respond to negative feedback of elevated calcium
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33
Q

Lab findings of hyperparathyroidism (primary)

A
  • Increased iCa
  • PTH (high or inappropriately normal)
  • Increased Vit D
  • Decreased phosphorus
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34
Q

Causes of granulomatous disease

A
  • disseminated fungal disease
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35
Q

Mechanism of hypercalcemia in Granulomatous disease

A
  • Increased Vit D levels via activated macrophages
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36
Q

Lab findings for Granulomatous disease

A
  • Increased Ca

- Normal or increased phosphorus

37
Q

Which neoplasias can lead to hypercalcemia?

A
  • Lymphosarcoma (esp T cell)
  • Multiple myeloma
  • Adenocarcinoma of anal sac and mammary glands, etc.
38
Q

What is the mechanism of hypercalcemia in neoplasia?

A
  • PTH-rp (related peptide)
39
Q

Lab findings for Neoplasia hypercalcemia

A
  • Increased iCa (and usually total)
  • Regular PTH will be inappropriately normal or decreased
  • Phosphorus decreased to normal
40
Q

What is the mechanism of hypercalcemia in renal disease?

A
  1. Decreased excretion of Phos, Ca, and PTH by poorly functional kidneys OR
  2. Renal secondary hyperparathyroidism
41
Q

Lab findings for renal disease (relevant to hypercalcemia)

A
  • Possibly high total Ca, usually normal iCa, PTH normal, Phosphorus high
42
Q

What is the mechanism of hypercalcemia in Vitamin D toxicosis?

A
  • Increased Ca and Phos bone release and intestinal absorption
43
Q

What can cause vitamin D toxicosis?

A
  • Cholecalciferol rodenticide, dietary supplements, Psoriasis cream, some plants
44
Q

Lab findings for Vitamin D toxicosis

A
  • High calcium and phosphorus
45
Q

Primary hyperparathyroidism definition

A
  • Excessive production of PTH by the parathyroid glands
46
Q

Primary hyperparathyroidism Causes (3, and which is most likely?)

A
  • Parathyroid Adenoma (most common)
  • Parathyroid Carcinoma
  • Parathyroid Hyperplasia
  • Can affect 1+ gland
47
Q

Typical age of Primary hyperparathyroidism

A
  • Middle aged to older
48
Q

Typical sex of PHP

A
  • No sex predilection
49
Q

Typical Breeds of PHP

A
  • Keeshonds

- Labs, Goldens, German Shepherds

50
Q

Will most dogs with PHP be clinical or not?

A
  • Most dogs with PHP are usually NOT CLINICAL
51
Q

Clinical signs of PHP if present

A
  • PU/PD
  • Lethargy/Weakness
  • Urinary signs: infections, calculi
  • Long standing hypercalcemia can lead to renal failure
52
Q

Typical physical exam findings for a dog with PHP

A
  • Most of the time normal

- Any signs present are often subtle or non-specific, related to urinary issues, or due to unrelated causes

53
Q

What cause of hypercalcemia would you expect in an older, apparently healthy dog with hypercalcemia?

A
  • More than likely going to have PHP
54
Q

What tends to be a unifying feature of dogs with hypercalcemia not due to PHP? (IMPORTANT)

A
  • Many other causes generally result in a sick to very sick dog
55
Q

CBC findings in PHP

A
  • Usually normal

- Small % may have mild anemia

56
Q

Chem panel findings in PHP

A
  • Hypercalcemia (All)

- Low or low normal phosphorus (most)

57
Q

UA findings in PHP

A
  • Isosthenuria or hyposthenuria
  • UTI
  • Evidence of calculi
58
Q

Typical Malignancy Panel with Primary HyperPTH

  • iCa
  • PTH
  • PTHrp (PTH related peptide)
A
  • iCa: high
  • PTH: normal
  • PTHrp: normal (AKA low)
  • Elevated iCa and inappropriately normal PTH is consistent with HyperPTH
  • Lack of PTHrp does not completely rule out neoplasia
59
Q

PHP further diagnostics

A
  • Abdominal radiographs, ultrasound, or CT
  • Thoracic radiographs or CT
  • Cervical ultrasound or CT
60
Q

Abdominal radiographs, ultrasound, or CT of an animal with PHP findings (possibly)

A
  • Nephroliths, cystic calculi

- stones are fairly common

61
Q

Thoracic radiographs or CT of an animal with PHP

A
  • Look for evidence of metastasis
62
Q

Cervical ultrasound or CT of an animal with PHP

A
  • A mass in the area of the thyroid glands supports PHP

- Parathyroids should be <3 mm but can be difficult to visualize

63
Q

Treatment for PHP if severely hypercalcemic (e.g. iCa >2)

A
  • Fluid therapy
  • Diuretics
  • Glucocorticoids
  • Bisphosphonates
  • Calcitonin
  • Can do surgery of affected glands (would likely want to stabilize first)
  • Radiofrequency heat ablation
  • Ethanol ablation
64
Q

Treatment for PHP if mild and not clinical

A
  • Monitor

+/- Can do surgery of affected glands (would likely want to stabilize first)

+/- Radiofrequency heat ablation

+/- Ethanol ablation

65
Q

Surgical management of PHP

A
  • Normal parathyroid glands may be atrophied due to constant negative feedback from overactive parathyroid gland PTH production
  • After surgery, hypocalcemia can occur until the glands recover
66
Q

What should you start before and after surgery to remove a PTH producing tumor

A
  • Start prophylactic calcitriol (vitamin D) therapy
  • Start 1-2 days prior to surgery
  • Slowly taper over 2-4 months by gradually increasing the time between doses
  • Short term Ca2+ supplementation (Ca carbonate AKA tums) and taper slowly over 2-4 months
  • Goal is to keep Ca2+ high enough tp prevent clinical signs (normal set point is also higher, so they can start showing clinical signs at a higher than normal set point)
67
Q

What would you worry about if you did not treat primary hyperparathyroidism?

A
  • If hypercalcemia is present long enough it can lead to renal failure
68
Q

Hypoparathyroidism definition

A
  • Cessation of parathyroid function
69
Q

Classic lab characteristics of hypoparathyroidism

A
  • Decrease in serum calcium and an increase in phosphorus
70
Q

Decreased secretion of PTH effect on bone

A
  • Reduced bone resorption of calcium and phosphorus
71
Q

Decreased secretion of PTH effect on kidneys

A
  • Decreased calcium, magnesium, and hydrogen ion reabsorption
  • Increased phosphorus, sodium, potassium, and amino acid reabsorption by the kidneys
72
Q

What are 4 potentials causes of HypoPTH?

A
  1. Suppressed secretion of PTH without destruction (e.g. trauma from surgery or other)
  2. Atrophy - sudden correction of chronic hypercalcemia (post-op parathyroidectomy for PHP)
  3. Iatrogenic - removal of parathyroid glands during removal of thyroid glands
  4. Idiopathic - destruction of parathyroid gland (Primary; suspected immune mediated destruction)
73
Q

Differentials for hypocalcemia

A
  • P = phosphate enemas
  • E = eclampsia
  • A = albumin decrease
  • C = chronic renal disease
  • E = ethylene glycol toxicity/acute kidney injury
  • P = PTH deficiency
  • A = Acute pancreatitis
  • I = intestinal malabsorption
  • N = nutritional (vit D deficiency)

and many more!!!

74
Q

HypoPTH more common in cats or dogs?

A
  • Dogs
75
Q

Average age of HypoPTH

A

4.8 years

76
Q

Sex predisposition in HypoPTH

A
  • Females more common than males
77
Q

HypoPTH Breeds

A
  • Poodles
  • Mini Schnauzers
  • German Shepherds
  • Labrador Retrievers
  • Terriers
78
Q

Timing of clinical disease in HypoPTH

A
  • Signs often present suddenly

- True course of disease is gradual in onset

79
Q

Two most common clinical signs of HypoPTH

A
  • Seizures prior to diagnosis (Common
  • 80%)
  • Intense facial rubbing/biting or licking paws (Common - 60%)
80
Q

Other clinical signs of HypoPTH

A
  • Tetany/muscles spasms
  • Tense/nervous
  • Stiff/stilted gait
  • Anorexia
  • Lethargy/weakness
  • Panting
  • Vomiting/Diarrhea
  • Cataracts
  • Fever
  • Growling
  • Cardiac abnormalities
81
Q

Changes on physical exam with HypoPTH

A
  • Muscle fasiculations
  • Seizures during exam
  • Cardiac abnormalities in up to 40% (Tachyarrhythmias, muffled heart sounds, weak pulses)
  • May not be contracting as well
82
Q

Diagnosis of HypoPTH based on labwork

A
  • Clinical signs = decreased serum Calcium
  • Rule out other dfdx
  • Increased serum Phosphorus
  • Ionized calcium decreased
  • PTH and calcitriol levels
83
Q

PTH and Calcitriol levels in HypoPTH

A
  • Parathyroid hormone low to low normal

- Decreased calcitriol

84
Q

Duration of treatment for HypoPTH

A
  • LIFELONG
85
Q

Emergency therapy for hypocalcemia (HypoPTH)

A
  • IV calcium gluconate
  • Give SLOWLY (10-30 minutes)
  • If given too quickly you can stop the heart
  • Subcutaneous administration an option after tetany is controlled
  • Use diluted 10% Ca Gluconate only
  • Potential risk of inflammation or skin sloughing
86
Q

Treatment for HypoPTH

A
  • Calcitriol (oral or injectable)
  • Generally lifelong
  • Oral calcium
  • Calcium carbonate - Tums
  • Can usually be tapered down or stopped after stabilization of disease
87
Q

Monitoring of HypoPTH

A
  • Frequent rechecks of iCa if necessary

- Every animal responds differently to calcitriol and dose and frequency adjustments are often needed

88
Q

Goal of HypoPTH therapy

A
  • Low normal or slightly low calcium levels

- Avoid hypercalcemia due to risk of renal failure and other complications

SA Medicine Endocrine (8 decks)

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