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Endocrine II midterm > Guerin: Parathyroid > Flashcards

Guerin: Parathyroid Flashcards

1
Q

Chief cells

A

-they secrete PTH

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2
Q

Oxyphil cells

A
  • acidophilic cytoplasm

- tightly packed with mitochondria

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3
Q

Function of the parathyroid

A
  • regulate calcium

- low calcium…. increased PTH

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4
Q

What does PTH do?

A
  • increased renal tubular reabsorption of calcium
  • increases urinary P excretion
  • Increases the conversion of Vit D to its active dihydroxy form in the kidney
  • release of calcium and P from bone
  • net result: raise level of free calcium, inhibit further PTH secretion
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5
Q

What are some causes of Hypercalcemia where PTH is elevated?

A
  • hyperparathyroidism

- familial hypocalciuric hypercercalcemia

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6
Q

What are some causes of hypercalcemia that have decreased PTH

A
  • hypercalcemia of malignancy
  • Vit D toxicity
  • Immobilization
  • thiazide diuretics
  • Granulomatous disease (sarcoidosis)
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7
Q

What is primary Hyperparthyroidism?

A
  • autonomous overproduction of parathyroid hormone (PTH)
  • Adenoma (85-95%)
  • hyperplasia of parathyroid tissue
  • rarely parathyroid carcinoma
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8
Q

What is secondary hyperparathyroidism?

A
  • compensatory hypersecretion of PTH in response to prolonged hypocalcemia
  • chronic renal failure
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9
Q

What is tertiary hyperparthyroidism?

A
  • Hypersecretion of PTH even after the cause of prolonged hypocalcemia is corrected
  • E.g. after renal transplant
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10
Q

Parathyroid adenoma

A
  • Cyclin D1 gene inversions… overexpression
  • MEN1 mutations… tumor suppressor gene
  • Famlilial syndromes: MEN1 and 2
  • familial hypocalciuric hypercalcemia
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11
Q

What mutation does MEN have?

A

-MEN1 or RET germline mutations

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12
Q

What is familial hypocalciuric hypercalcemia

A
  • rare auto dominant

- mutations in the parathyroid calcium-sensing receptor gene (CASR)

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13
Q

Morphology of the adenoma

A
  • solitary
  • well-circumscribed
  • glands outside the adenoma are usually normal or shrunken from feedback inhibition by elevated calcium
  • hpercellular with little to no fat
  • composed of uniform chief cells
  • few nests of larger oxyphil cells…. occasionally composed entirely of them
  • usually a rim of compressed, parathyroid fland, generally separated by a fibrous capsule
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14
Q

Parathyroid hyperplasia

A
  • occurs sporadically or as a component of MEN syndrome
  • calssically ALL FOUR GLANDS INVOLVED
  • HYPER CELLULAR WITH LITTLE TO NO FAT
  • TYPICALLY SEE CHIEF CELL HYPERPLASIA
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15
Q

Parathyroid carcinoma

A
  • rare
  • cells can look like normal parathyroid
  • need invasion of surrounding tissues and/or metastasis for dx
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16
Q

Sestamibi scan

A
  • radionucleotide scan

- Sestamibi labeled with the radi-pharmaceutical technetium-99

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17
Q

What are Brown tumors?

A
  • microfactures and secondary hemorrhages…. influx of macrophages and reparative fibrous tissue…. mass lesion in bone
  • brown color from vascularity, hemorrhage, and hemosiderin deposition
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18
Q

What is osteitis fibrosa cystica?

A
  • increased osteoclast activity, peritrabecular fibrosis, and cystic brown tumors
  • severe hyperparathyroidism, rare
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19
Q

What happens with the other organs in hyperparathyroidism?

A

-calcification!

20
Q

What is the most common cause of hyperparathyroidism?

A

malignancy

21
Q

Hypercalcemia of malignancy?

A
  • most common cause of symptomatic hypercalcemia
  • solid tumors
  • hematologic malignancies: multiple myeloma
  • typically caused by tumor secretion of PTH-related peptide (PTHrP)… it acts like PTH
  • can also be from metastases to the bone and subsequent cytokine-induced bone resorption
22
Q

What are the labs for primary hyperparathyroidism?

A
  • high calcium levels
  • high PTH…. but remember that PTH is low in hypercalcemia causes by non-PT diseases
  • hypophosphatemia
23
Q

Symptoms of primary hyperparathyroidism

A
  • bones, stones, (abdominal) groans, and (psychic) moans
  • bone problems
  • nephrolithiasis
  • GI sx: constipation, nausea, peptic ulcers, pancreatitis, and gallstones
  • CNS sx: depression, lethargy, and eventually seizures
  • NM weakness and fatigue
  • Cardiac: aortic or mitral valve calcifications
24
Q

Secondary Hyperparathyroidism

A
  • caused by any condition that leads to chronic hypocalcemia…. overactive parathyroid glands
  • usually renal failure
  • inadequate dietary intake of calcium, steatorrhea, and vitamin D deficiency
  • mechanism is not fully understood but related to high serum phophate
25
Q

Morphology of secondary hyperparathyroidism

A
  • hyperplastic parathyroid glands
  • increased number of chief cells
  • “metastatic” calcifications can be seen in lungs, heart, stomach, and blood vessels
26
Q

Clinical course of secondary hyperparathyroidism

A
  • sx not as severe or as prolonged as primary hyperparathyroidism
  • Calciphylaxis: vascular calcification… ischemic damage to skin and other organs
27
Q

Tx of secondary Hyperparathyroidism

A

-Vit D supplements and phosphate binders

28
Q

Tertiary hyperparathyroidism

A
  • occasionally in pt with secondary hyperparathyroidism

- parathyroids become autonomous and excessive

29
Q

Tx of teriary hyperparathyroidism?

A

-removal of parathyroids

30
Q

If there is elevated PTH, what will serum calcium and Phosphate look like?

A
  • High calcium

- Low phosphate

31
Q

Hypoparathyroidism

A
  • uncommon
  • surgically induced
  • autoimmune
  • auto dominant
  • Familial isolated
  • congenital absence of the parathyroid glands
32
Q

What is autoimmune hypoparathyroidism associated with?

A

chronic mucocutaneous candidiasis and primary adrenal insufficincy
-called autoimmune polyendocrine syndrome type 1 APS1

33
Q

What is Autosomal-dominant hypoparathyroidism?

A

-GOF in the calcium sensing receptor (CASR) gene

34
Q

Clinical manifestations of hypocalcemia

A
  • tetany
  • numbness and paresthesias of distal extremities
  • Chvostek sign
  • Trousseau sign: carpal spasms produced by occlusion of circulation tot he forearm
  • Mental status changes: anxiety and whatnot
  • Heart: prolonged QT
  • Dental abnormalities when hhypocalcemia is present during early development
35
Q

What is a weird finding in hypocalcemia?

A
  • paradoxical calcifications
  • Lens and cataract formation
  • Basal ganglia…. parkinsonian-like movement disorder
36
Q

Pseudohypoparathyroidism

A
  • end organ resistance to PTH
  • serum PTH levels are normal or elevated
  • presents as hypocalcemia and hyperphosphatemia
  • can also have end-organ resistance to PTH, TSH, and FSH/LH (from genetic defects in G ptn coupled receptors
37
Q

What is the most common cause of asymptomatic hypercalcemia

A

-primary hyperparathyroidism

38
Q

In the majority of cases, what is primary hyperparathyroidism caused by?

A
  • sporadic parathyroid adenoma

- less commonly by hyperplasia

39
Q

Parathyroid adenomas vs. Hyperplasia

A
  • adenomas: solitary

- hyperplasia: multiglandular process

40
Q

What are the skeletal manifestations of hyperparathyroidism?

A

-bone resorption
-osteitis fibrosa cystica
-brown tumors
(renal changes: stones and nephrocalcinosis)

41
Q

What are the clinical manifestations of hyperparathyroidism?

A
  • bones
  • stones
  • groans
  • psychic moans
42
Q

What is secondary hyperparathyroidism most often caused by

A
  • renal failure

- lowers serum calcium levels, resulting in reactive hyperplasia of parathyroid glands

43
Q

What is the most important cause of symptomatic hypercalcemia?

A
  • malignancies

- results from osteolytic metastases or release of PTHrP from non-parathyroid tumors

44
Q

How is hypoparathyroidism most commonly induced?

A

surgically

45
Q

What are the classic signs of hypoparathyroidism?

A
  • tetany
  • Mental status changes
  • prolongation of QT interval

Endocrine II midterm (13 decks)

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