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Flashcards in Parathyroid - Shaker Deck (30):

Give some signs and symptoms of hypocalcemia

  • Neuromuscular irritability - parathesias, cramps, tetany
  • Lowered seizure threshold
  • Mental status changes
  • Cardiac symptoms - prolonged QT, arrhythmias, CHF
  • Basal ganglia calcification
  • Cataracts
  • Positive Chvostek's and Trousseau's signs


What is the Chvostek sign?

Clinical sign of nerve hyperexcitability seen in hypocalcemia

(Wiki): When the facial nerve is tapped near the angle of the jaw, the facial muscles on the same side as the tapping will momentarily contract


What is Trousseau's Sign?

A sign observed in patients with hypocalcemia

Wiki: a blood pressure cuff placed around the arm and inflated to above systolic pressure (such that the brachial artery is occluded) for several minutes, the muscles of the forearm and hand will spasm (finger adduction, MCP flexion, PIP/DID extension)


Hypocalcemia caused by a deficiency in PTH secretion is called what?

Hypocalcemia resulting in an increase in PTH secretion is called what?

Primary hypoparathyroidism

Secondary hyperparathyroidism


What cause of hypocalcemia is caused by resistance to PTH?



Hypoparathroidism: increased, normal, or decreased?

  • Serum calcium
  • Serum phosphate
  • Intact PTH
  • 25-(OH)D3

  • Decreased
  • Increased or normal
  • Decreased or normal
  • Normal


Pseudohypoparathyroidism: increased, normal, or decreased?

  • Serum calcium
  • Serum phospate
  • Intact PTH
  • 25-(OH)D3

  • decreased
  • increased or normal
  • increased
  • normal


Magnesium depletion: increased, normal, or decreased?

  • Serum calcium
  • Serum phospate
  • Intact PTH
  • 25-(OH)D3

  • decreased
  • normal
  • decreased or normal
  • normal


Secondary hyperparathyroidism: increased, normal, or decreased?

  • Serum calcium
  • Serum phospate
  • Intact PTH
  • 25-(OH)D3

  • decreased
  • normal or decreased
  • increased
  • decreased


What is the genetic mutation associated with type 1a pseudohypoparathyroidism?

Autosomal dominant or autosomal recessive?

What is the usual clinical presentation?


Autosomal dominant

Albright's Hereditary Osteodystrophy (AHO):

  • Short stature
  • Short 4th and 5th metacarpals
  • rounded facies
  • mild mental retardation


In the setting of hypocalcemia, what is likely to be the best first test to order?

  • If PTH is elevated with normal to low serum phosphate, what is the differential? What are appropriate next steps?
  • If PTH is elevated with high serum phosphate, what is the differential now?
  • If the PTH is decreased or inappropriately normal, what is the differential now?

serum PTH levels

  • Consider vitamin D insufficiency or occult malabsorption. Measure 25(OH) vitamin D and measure 24hour urine calcium and creatine. Consider serologic screening for celiac disease and BMD measurement.
  • Consider PTH resistance or renal insufficiency
  • Probably hypoparathyroidism, but first r/o magnesium deficiency (reversible hypoparathyroidism)


Explain the difference between the management strategies for acute and chronic hypocalcemia

  • Acute: initial management with IV calcium gluconate
  • Chronic: if due to hypoparathyroidism, treat with calcium supplements and vitamin D2 or D3 or calcitriol


FGF23 (Fibroblast growth factor 23)

  • Cell of origin?
  • Effects?
  • What is the consequence of excess FGF23?
  • What is the consequence of reduced FGF23?

  • Made by osteocytes (bone cells)
  • Effects: increase urinary phosphate excretion and decreased renal production of 1,25(OH)2D
  • Excess causes hypophosphatemia and impaired bone mineralization
  • Decreased casues hyperphosphatemia and tumoral calcinosis


Give (4) broad causes of hypophosphatemia

  1. Reduced renal tubular reabsorption (such as excess FGF23)
  2. Impaired intestinal phosphate absorption
  3. Shifts of extracellular phosphate into cells (insulin therapy, catecholamines, tumors, respiratory alkalosis)
  4. Accelerated net bone formation


Give five broad causes of hyperphosphatemia

  1. Impaired renal phosphate excretion (renal insufficiency, hypoparathyroidism, pseudohypoparathyroidism)
  2. Vitamin D intoxication
  3. Sarcoidosis or other granulomatous diseases
  4. Massive extracellular fluid phosphate loads (rapid IV/oral/rectal, cellular injury/necrosis)
  5. Transcellular phosphate shifts (metabolic or respiratory acidosis)


What are the source and site of storage of calcium?

How is it transported in blood?

Absorbed in the GI (mostly duodenum and jejunum), stored in bony mineral matrix.

About half of plasma calcium is protein-bound.


What is the chief regulator of serum calcium?

Describe its release and effect.

Parathyroid hormone

Parathyroid chief cells detect calcium levels via the CaSR. The PTH (and PTHrP) receptor activates Gs/cAMP and/or Gq/PLC pathways, depending on the target tissue.


Name 4 effects of PTH on calcium.

Increases kidney reabsorption

Increases gut absorption

Increases bone resorption

Promotes 1-hydroxylase in kidney to produce calcitriol (in turn promoting gut absorption)


Describe how vitamin D is activated and eventually inactivated.

D2 and D3 are 25-hydroxylated in the liver (non-regulated), and then 1-hydroxylated in the kidneys (under control of PTH). The resulting 1,25-dihydroxyD (calcitriol) is inactivated by 24-hydroxylation.


Relate some of the symptoms of hypercalcemia. Which is most common?

Fatigue & weakness

Nausea, vomiting, constipation & anorexia

Polyuria (& polydipsia)

Memory impairment, drowsiness, confusion, coma.

Dehydration (due to anorexia/vomiting as well as renal salt loss)

*Most patients are asymptomatic!


Name some etiologies of a PTH-dependent hypercalcemia.

Sporadic adenoma


"Hyperparathyroid jaw tumor syndrome"

Familial isolated hyperparathyroidism

Familial hypocalciuric hypercalcemia

Ectopic PTH (very uncommon)


What lab findings are seen in primary hyperparathyroidism?

Increased or inappropriately normal PTH & decreased sensitivity of plasma calcium (of course)

Hypercalcemia due to PTH overload

Hypophosphatemia due to phosphaturic effects of PTH in proximal tubules.

Sometimes hypercalciuria (renal calcium reabsorption is increased, but can still be overwhelmed)


Contrast FHH's presentation with other primary hyperparathyroidisms.

It is asymptomatic, with modest hypercalcemia and no indication for surgical treatment.

Hypocalciuria (reabsorption not overwhelmed)

PTH not suppressed (this is obvious and non-distinguishing)


What is the most common form of FHH?

FHH1, in which the CaSR gene on chromosome 3 is mutated. It has an autosomal dominant/codominant effect, causing hyperparathyroidism.

Note: FHH2/3 presumably aren't due to CaSR mutations.


What bony manifestations are seen in hyperparathyroidism?

Hyperpara Osteitis - Also known as Osteitis fibrosa cystica. Bone is replaced with fibrous tissue ("peritrabecular"). 

Brown tumors - Lesions comprised of normal bony tissue (fibrous, vascular, woven) without matrix.

Cortical bone wasting - Worse than trabecular...


Name 2-3 major causes of PTH-independent hypercalcemia.

Cancer, sarcoid/calcitriol elevation, hyperparathyroidism

(minor: Calcium-alkali syndrome, immobilization)


What is PTHrP, and what is its relevance to hypercalcemia?

A hormone that functions like PTH (and indeed shares structural homology), normally important to fetal development.

It is a marker for hypercalcemia resulting from malignancy (breast, lung, kidney, etc). Note that it does not appear on PTH assays (and therefore is PTH-independent).


Say a patient presents with serum calcium of 11. You run a serum PTH and find that it is markedly elevated.

Diagnosis? Next steps?

This is probably a primary hyperparathyroidism. Since FHH can resemble it, measure urine creatinine & calcium over a 24hr period (check for hypercalciuria, renal function)


Basic treatment of any hypercalcemia includes IV fluids and loop diuretics. Explain why.

Fluids - Patients are usually dehydrated due to nausea/vomiting/diarrhea and renal losses.

Loop diuretics - Promote calcium excretion and balance volume expansion due to fluid treatment.


Name 3 drugs (besides diuretics & saline) used to treat hypercalcemia, and why they are employed.

Calcitonin - Opposes PTH, should lower serum calcium, reduce bone resorption, etc.

Bisphosphates - Inhibit osteoclastic bone resorption

Cinacalcet - Calcimimetic; reduces PTH secretion (assuming the adenoma is only semi-autonomous)

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