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Endo > Parathyroid Gland > Flashcards

Parathyroid Gland Flashcards

1
Q

Describe how calcium is absorbed:

A
  • GI Calcium Absorption
    • 20-70% (highest in children)
    • 90% in duodenum and jejunum
  • Energy-dependent, cell-mediated process regulated by 1,25(OH)2D
  • Passive diffusional paracellular pathway
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2
Q

Describe how plasma calcium is increased:

A

low plasma Ca2+ ⇒ ↑ PTH from parathyroid chief cells

  • PTH ⇒ ↑ plasma calcium
    • ↑ Ca2+ kidney reabsorption
    • ↑ Ca2+ intestinal absorption
    • ↑ Ca2+ bone resoprtion
  • PTH ⇒ ↑ conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D
  • 1,25-dihydroxyvitamin D ⇒ ↑ Ca2+ intestinal absorption
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3
Q

Describe the negative feedback for PTH:

A

High plasma Ca2+ ⇒ ↓ PTH secretion

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4
Q
  • What senses calcium?
    • Loss of function ⇒
    • Gain of function ⇒
  • What can be used to treat severe hyperparathyroidism?
A
  • Calcium Sensing Receptor (CaSR) senses calcium (expressed in parathyroid gland, kidney etc)
    • Loss of function ⇒ familial hypocalciuric hypercalcemia (FHH)
    • Gain of function ⇒ autosomal dominant hypocalcemia (ADH)
  • Calcimimetic (cinacalcet) can be used to treat severe hyperparathyroidism
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5
Q
  • What are the diffrent vitaminD forms?
  • How are they activated?
A
  • Vitamin D2 (plant vitamin D or ergocalciferol) consumed
  • Vitamin D3 (made in skin or consumed - cholecalciferol)

Activation

  1. UV light converts the cholesterol derivative
  2. Both 25-hydroxylated to 25(OH)D at liver in a largely unregulated step (genetic variants may effect this step)
  3. Both then 1-hydroxylated in kidney to 1,25(OH)2D in a highly regulated step stimulated by PTH
  4. 24-hydroxylase deactivates 25D
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6
Q

Symptoms of Hypercalcemia

A
  1. Fatigue, weakness
  2. Nausea, vomiting, constipation
  3. Anorexia
  4. Polyuria, polydipsia
  5. Dehydration
  6. Memory impairment
  7. Drowsiness, confusion, coma
  8. Most ambulatory patients - no clear sx
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7
Q
  • What can cause hypercalcemia (as it’s related to PTH)?
  • What can hypercalcemia result in?
A
  • Hypercalcemia is caused by an increase in PTH secretion
    • Primary hyperparathyroidism
      • usually a parathyroid adenoma
  • Hypercalcemia results in a **suppression of PTH secretion **
    • Vitamin D intoxication, Hypercalcemia of malignancy
      • caused by PTHrp
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8
Q

Examples of PTH dependent hypercalcemia:

A
  • Primary hyperparathyroidism (PHPT)
    • Sporadic (single and multiple gland disease, carcinoma)
    • Multiple endocrine neoplasias (MENs)
    • Hyperparathyroidism jaw tumor syndrome
  • Familial isolated hyperparathyroidism
  • Familial hypocalciuric hypercalcemia (FHH)
  • Ectopic PTH – RARE!
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9
Q

Primary Hyperparathyroidism:

Physiologic Findings

A
  • Decreased sensitivity of PTH-secreting cells to inhibition by plasma Ca2+
  • Increased or “inappropriately not suppressed” serum PTH levels
  • Hypercalcemia
    • bone resorption
    • calcium reabsorption
    • increase in 1,25(OH)2D production
  • Hypophosphatemia
    • phosphaturic effects of PTH in the proximal tubules
  • Some patients are hypercalciuric despite PTH mediated increase in Ca2+ reabsorption in the distal tubules because the filtered load of calcium exceeds the TM for reabsorption
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10
Q

Familial Hypocalciuric Hypercalcemia (FHH):

  • Symptoms
  • Urine calcium
  • PTH activity
  • Inheritance?
  • Surgery?
A
  • Asymptomatic, modest, lifelong hypercalcemia
  • Hypocalciuria
  • PTH not suppressed
  • Autosomal dominant
  • Surgery not indicated
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11
Q

Familial Hypocalciuric Hypercalcemia:

Genetics

A
  • FHH1: Most families - CaSR (chromosome 3) (~2/3)
    • Codominant - neonatal severe hyperparathyrodism
  • Recent discovery of FHH2 and FHH 3 genes
  • Not all FHH have CaSR mutations
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12
Q

Describe the effects on the skeleton in “typical” PHPT:

A
  1. It is not known if the relationship between BMD and fractures in PHPT similar to that in osteoporosis
  2. Baseline BMD is more decreased at cortical sites with relative sparing of trabecular bone; subset with spinal osteopenia (~15%).
  3. Fractures may be increased
  4. Newer techniques suggest trabecular bone may not be normal
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13
Q

Causes of PTH-independent Hypercalcemia:

A
  • Malignancy
    • Bone metastases, PTH-related protein, Osteoclast activating factors, Unregulated calcitriol production, True ectopic PTH
  • Calcitriol-mediated (granulomatous, inflammatory)
    • Calcitriol is a synonym for 1,25(OH)2D
  • Hyperthyroidism
  • Milk-alkali syndrome or calcium-alkali syndrome
  • Immobilization
  • Rare causes
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14
Q

What is Parathyroid-Hormone-Related
Peptide (PTHrP)?

A
  • Humoral hypercalcemia of malignancy
    • breast, lung, kidney, squamous etc.
  • N-terminal homology with PTH
  • Not measured on PTH assays
  • PTHrP assays available
  • PTHrP found in normal tissue/high concentrations in milk
  • PTHrP important in fetal development
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15
Q

What are causes of calcitriol (1,25[OH]2D)-mediated hypercalcemia?

A

Non-renal/unregulated expression of 1-hydroxylase

  • Sarcoid
  • Lymphoma
  • Tuberculosis
  • Other less common conditions
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16
Q

What should be checked first if a patient has hypercalcemia?

A

PTH levels!

17
Q

What is the most likely diagnosis if a patient has hypercalcemia + ↑ PTH (or “inappropriately not suppressed”)?

  • What should be done from here?
  • Why is there hypercalcemia in this patient?
A

Most likely dx – primary hyperparathyroidism

  • Measure 24 hour urine calcium & creatinine
    • to rule out FHH
  • A primary process causing too much PTH (primary hyperparathyroidism)
    • will cause hypercalcemia
      • increased bone resorption
      • increased production of 1,25(OH)2D)
18
Q

What are the possible outcomes if a patient has hypercalcemia + suppressed PTH?

  • When should further invesigation be conducted?
  • What is the reason for suppressed PTH?
A

Possibilities: Known malignancy, obvious cause, no known cause

  • If there is no known cause, evaluate for:
    • Excess 1,25D
      • eg sarcoid tumor
    • Cancer
    • Hyperthyroidism
    • Less common conditions
  • A process which raises the serum calcium independent of PTH (for example a tumor producing PTH related protein or lytic bone lesions) will suppress PTH
19
Q

What is treatment for hypercalcemia?

A
  • Calcitonin – a rapid reduction in Ca2+ can occur
    • “Escape” from the hormone commonly occurs within several days
    • Can lower serum calcium by 1-2 mg/dL
  • Bisphosphonates – IV
    • potently inhibit osteoclastic bone resorption
  • IV fluids – Normal saline
  • Loop diuretics – Furosemide
    • Monitor for electrolyte balance
20
Q

Signs and Symptoms of Hypocalcemia:

A
  • Neuromuscular irritability
    • paresthesias, muscle cramps, tetany
  • Positive Chvostek’s and Trousseau’s signs
  • Lowered seizure threshold
  • Mental status changes
  • Cardiac - prolonged QT, arrhythmias, CHF
  • Basal ganglia calcification
  • Cataracts
21
Q
  • What can cause hypocalcemia (as it relates to PTH)?
  • What does hypocalcemia result in?
A
  • Hypocalcemia is caused by a deficiency in PTH secretion
    • Primary hypoparathyroidism (iatrogenic, idiopathic, or familial)
  • Hypocalcemia results in an increase in PTH secretion
    • Secondary hyperparathyroidism (very common
      • renal failure
      • Vitamin D deficiency – cannot produce adequate 1,25(OH)2D]
      • malabsorption
22
Q
  • What are the four different lab manifestations of hypocalcemia?
  • What are the lab findings for each?
A
  1. Primary Hypoparathyroidism
  2. Pseudohypoparathyroidism
  3. Mg2+ depletion
  4. Secondary Hyperparathyroidism
23
Q

Hypoparathyrodism can be due to ….

A
  • Genetic disorders
  • Autoimmune
  • Infiltrative
  • Pseudohypoparathyroidism (PTH resistance)
    • Type 1a has GNAS mutation and Albright’s Hereditary Osteodystrophy (AHO)
24
Q

What is the first thing that should be checked if a patient has hypocalcemia?

A

PTH levels!

25
Q

What is the most likely diagnosis if a patient has hypocalcemia + ↑ PTH with normal to low serum phos?

  • What are the possible causes of this manifestation?
  • What further workup can be done?
A

Most likely dx – Secondary hyperparathyroidism

  • Possible Causes:
    • vitamin D insufficiency
    • occult malabsorption
  • Further workup:
    • Measure 25(OH) vitamin D
    • Measure 24 hour urine calcium & creatinine
    • Consider serologic screening for celiac disease
    • Consider BMD measurement
26
Q

What is the most likely diagnosis in a patient with hypocalcemia + ↑ PTH with high phos?

A
  • Differential diagnosis:
    • Pseudohypoparathyroidism (PTH resistance)
    • Renal insufficiency
27
Q

What is the most likely diagnosis in a patient with hypocalcemia + ↓ or normal PTH?

A
  • probable primary hypoparathyroidism
  • rule out magnesium deficiency
28
Q

Treatment of Hypocalcemia:

  • Acute hypocalcemia
  • Chronic hypocalcemia due to hypoparathyroidism
A
  • Acute hypocalcemia
    • initially managed with IV calcium gluconate
  • **Chronic hypocalcemia due to hypoparathyroidism **
    • treated with calcium supplements and either vitamin D2 or D3 or calcitriol
29
Q
  • What makes FGF23?
  • What are the effects of FGF23?
  • What happens if there is excess FGF23?
  • What happens if there is decreased FGF23 activity?
A
  • FGF23 made by bone cells (osteocytes)
  • Effects:
    • increases urinary phosphate excretion
    • decreases renal production of 1,25(OH)2D
  • Excess FGF23 ⇒ hypophosphatemia and impaired bone mineralization
    • genetic forms of rickets
    • tumor- induced osteomalacia
  • Decreased FGF23 action ⇒ hyperphosphatemia and tumoral calcinosis
30
Q

What are causes of Hypophosphatemia?

A
  • Reduced renal tubular phosphate reabsorption
    • PTH/PTHrP-dependent
    • PTH/PTHrP-independent
      • Excess FGF23 or other “phosphatonins”
      • Intrinsic renal disease that causes phos wasting
  • Impaired intestinal phosphate absorption
  • Shifts of extracellular phosphate into cells
    • Intravenous glucose
    • Insulin therapy for prolonged hyperglycemia or diabetic
    • ketoacidosis
    • Catecholamines (epinephrine, dopamine, albuterol)
    • Acute respiratory alkalosis
    • Rapid cellular proliferation
  • Accelerated net bone formation
31
Q

What are causes of Hyperphosphatemia?

A
  • Impaired renal phosphate excretion
    • Renal insufficiency
    • Hypoparathyroidism
    • Pseudohypoparathyroidism
    • Tumoral calcinosis
  • Vitamin D intoxication
  • Sarcoidosis, other granulomatous diseases
  • Massive extracellular fluid phosphate loads
    • Rapid administration of exogenous phosphate (intravenous, oral, rectal)
    • Extensive cellular injury or necrosis
  • Transcellular phosphate shifts
    • Metabolic acidosis
    • Respiratory acidosis

Endo (18 decks)

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